- Hippopotamus
- Hippopotamus amphibius :
- contamination of grazing, generally as a result of an infected animal carcass leaking infected blood from its orifices onto the pasture.
- ingestion of contaminated water, particularly in small stagnant pools that are drying up during dry periods. In this situation, the infection appears to be related to stress, stagnation (no diluting or flushing of spores), and relative overpopulation. Most outbreaks of anthrax in Africa occur during the dry season or dry cycles.
- open wound lacerations resulting in per-cutaneous infections. This route of infection may possibly even occur in larger expanses of water, where there is a dilution factor, but is more likely to occur in smaller stagnant pools that have become heavily contaminated.
- cannibalism with ingestion of tissues from an infected carcass.
- anthrax is endemic in many areas of Africa and the world, and these endemic areas are frequently associated with alkaline soils and alkaline surface water frequently related to volcanic /calcite geological formations. The Queen Elizabeth system fulfills most of these criteria.
- in the Bacillus anthracis life cycle, long dormant periods in the environment in the resistant spore survival mode are interspersed with short periods of exponential replication of the germinated bacilli within suitable hosts during outbreaks. Interepidemic periods may be measured in years or decades, and in remote areas of the developing world, the disease may not have been previously recognised or documented.
- triggers for these outbreaks include local overabundance of hosts, poor soil drainage and stressors generally associated with resource depletion and intra- and inter-specific competition. Hippos have few natural enemies except man, and there is a cyclical tendency for their population growth to exceed the ecological carrying capacity of their nocturnal grazing range. Dry seasons and dry cycles compound the problem. In the Queen Elizabeth National Park system, Lake Edward and Lake George (linked by the Kazinga channel) are major aquatic features stretching for many square miles, and support a large hippo population. Census figures in 1958 reported a population in excess of 15 000 for the system, with resultant severe overgrazing, trampling and soil erosion. Between 1958 and 1966, more than 7000 hippos were culled to address this overabundance issue. A 1969 census showed that there were still 10 000 hippos in the system. Heavy poaching in the 1970s reduced this population by half, but by the 1990s the population had recovered again to over 7500. I unfortunately have no recent census figures.
- anthrax outbreaks may possibly be seen as a natural population-regulating mechanism for some species (including hippos) under certain environmental conditions and relative population density situations. Epidemic outbreaks are relatively short-lived (generally measured in months) and in most species (except buffalo and bison) there appears to be no gender predilection. The male predilection seen in African buffalo and bison appears to be linked to wallowing behaviour. Another observation is that sub-adult animals are relatively under-represented in carcass counts.
- contamination of grazing by the leaking of unclotted blood from body orifices of terminal or dead individuals and from scavenged freshly dead carcasses.
- contamination of lake shallows and pools and cattle troughs by bathing vultures that have recently fed on infected carcasses.
- percutaneous infection of fight wounds by spores in the environment or spores in the oral cavity of the aggressor.
- mechanical transmission by large haematophagous biting flies (Pangonia spp.) which target hippos.
- cannabalism with ingestion of tissues from infected carcasses.
- vaccination of endangered wildlife species that are at risk -- as many as possible -- where possible.
- public awareness campaigns stressing the danger of handling or utilising carcasses of dead animals.
- reduction of contamination of the environment by burning or [2nd best] burying carcasses. Alternately, making carcasses unattractive to scavengers by spraying with formalin or covering with branches or sheets of plastic until putrefaction, anaerobic conditions, acid pH and temperature destroy the bacilli in the carcass (2- 4 days). About 10 years ago, the Canadians discovered in the MacKenzie Bison Sanctuary that one could prevent carcass scavenging long enough for decomposition to change the pH -- and thereby kill the vegetative organisms -- by spraying carcasses with 5% formaldehyde. This acid pH change takes only a few days (3 to 5 days), after which a carcass can be left to rot and nature with minimal environmental contamination. If the fresh carcass is not opened, minimal or no sporulation occurs. In the case of hippopotami, their aquatic habits frequently result in the carcasses of anthrax victims floating or surrounded by shallow water, making them relatively inaccessible to winged or terrestrial scavengers. Their thick hide is not easily penetrated (even by crocodiles) until putrefaction is fairly advanced. Most bacilli in the carcases will therefore be destroyed by their anaerobic and acidic environment together with the massive growth of putrefactive organisms. Theoretically therefore, floating hippo carcasses should not be a major source of contamination by spores, with the exception of exudates from orifices (when present). Also, in the main bodies of water of large lakes, the dilution factor for spores should be such as to pose minimum risk. However, contamination of small pools and inlets will probably require the removal, beaching and burning or burying of carcasses.
Bacillus anthracis
in Southern Africa is generally regarded to be sporadic in hippopotamiref.
An abnormally high mortality among hippos was observed in the Luangwa River
valley, Zambia, in 1987. It was estimated that between June and November
2004, > 4000 deaths were attributed to anthrax. The enzootic status of
the region was confirmed by a field study in 1989ref.
> 200 hippos in 2004 and 23 hippos in 2005 died of anthrax in the Queen
Elizabeth National Park in Uganda, and surrounding livestock at risk have
been vaccinated. As it is not unusual to find cattle being grazed within
National Park boundaries in Africa this is patently a wise thing to do.
In some cases mortality may be the result of the communal scavenging or
"cannibalism" of carcasses of anthrax-killed hippos by other hippos, an
hypothesis appears to be supported by the apparent absence, until quite
recently, of any contemporaneous reports of anthrax deaths among buffalo
or other common wildlife host species, first reported in 1996 (both of
which involved hippos consuming meat from scavenged impala carcasses and
one of which involved a communal feeding episode), then from Lake Malawi
and 2 instances from Tanzania of hippos consuming scavenged wildebeest
carcasses. Video footage from the Luangua Valley of a hippo eating the
gut contents and/or internal organs of a dead buffalo. Mortality in hippos
can be caused by various other infectious, non-infectious, and toxic agents.
There is only one strain of Bacillus anthracis found essentially
in only one species, and that is the one associated with wood bison in
northern Alberta and the Canadian North West Territories. The issue is
not so much species-dependence as behavior-dependence. In those Canadian
areas, there are very few other target species sharing the wood bison areas;
the caribou are elsewhere; wolves have disappeared for unknown reasons;
and only the occasional moose will be affected, as it prefers to feed in
flooded areas. In areas where there is scrub, blow flies and browsers are
involved (i.e. kudu or white tailed deer); grazing animals in open savannah
are rarely afflicted. With these hippos, there is contaminated water involved
as well as, apparently, feeding on infected carcasses. In Africa, contaminated
water, whether in river ponds or in artificial troughs, has long been seen
as a risk to wild and domestic ruminants drinking there. But, with the
activity, they may well be going elsewhere to drink. The outbreaks of anthrax
in hippos in most African ecosystems appear to be density-related. Excessive
densities may be relative (when resources are scarce, as in drought) or
absolute, following optimal climatic conditions when resources are abundant,
and reproductive success and recruitment are high. Excessive densities
frequently result in resource depletion, increased competition, and intra-specific
aggression and conflict. Hippos can be extremely aggressive, and fights
frequently leave the combatants with numerous lacerations, and may be fatal.
Hippo cannibalism has occasionally been reported from different parts of
Africa but is rare and appears to be triggered by stress-induced "displaced"
behavior, or possible nutritional deficiencies or needs. Hippos have a
well developed (partially fermenting) foregut, but they are not ruminants.
They also have a very well developed (fermenting) hindgut (similar to rhinos
and elephants), hardly the digestive anatomy that one would expect in an
evolved omnivore. With regards to anthrax infection of hippos, there are
multiple mechanisms and routes involved, namely:
Hippos' secretions all over their back, face and behind their ears are neither blood nor precisely sweat, but a mixture of pigments (one red and one orange, christened hipposudoric acid and norhipposudoric acid) that function as both ultraviolet sunscreen and antibiotic for Pseudomonas aeruginosa and Klebsiella pneumoniae, as well as keeping the animals cool. The hippos tend to produce more of the substance when they are on dry land rather than swimming in rivers or lakes, bolstering the idea that the secretions are akin to sweat. But other experts have suggested that it functions as waterproofing; adults can remain submerged for > 5 minutes at a time. Such a dual function would be useful to the huge beasts, which live in central Africa, largely in the Nile Valley. They spend a lot of time in direct sunlight, and frequent fierce clashes with rival hippos leave them scarred and potentially vulnerable to infection. In isolation, the newly discovered compounds are very unstable, but hippos can retain their blood-red hue for several hours before losing their lustre thanks to the mucus secreted with the pigments may delay their discolourationref
- Bovidae
- Antilocapridae
- Antilocapra
- Antilocapra americana (pronghorn antelope)
- Bovinae
- Bison
- Bison bison (American bison)
- Bos
- Bos frontalis (gaur) are found in central and southern India, in Nepal & Bhutan, and in SE Asiaref
- Bos grunniens (domestic yak)
- Bos indicus (zebu)
- Bos primigenius (aurochs)
- Bos primigenius indicus (dwarf zebu) : a type of Asiatic ox that has a fleshy hump, floppy ears, a loose dewlap, and is highly resistant to the effects of heat and insect attack
- Bos taurus (cows, bovines, cattle) : cattle normally ingest 2-3 (up to 10) kg of soil per day
- Russia : places with any history of anthrax are permanently labelled as 'anthrax sites' :
- the Ural Federal region is approximately 1.8 million km2 in area, with a human population of about 12.5 million. The region consists of Kurgan, Sverdlovsk, Tumen, Chelyabinsk, Yamalo-Nenetskaya, and Hanti-Mansiyskaya national districts. The entire region (north to south) has a history of anthrax, and therefore the discovery of numerous anthrax sites (at least 2086) should not come as a surprise. At 4 of these sites, cases of animals being infected with anthrax were recorded between 1991 and 2000. In reality, the number of cattle gravesites is much higher, as there may be several such gravesites at any one of these anthrax sites. However, it is hard to say that there are positively identified anthrax spores in these gravesites -- as there have never been such investigations into these sites. The Tobolski gravesite, on the banks of the Irtish river, is peculiar, as it is the result of activity at a nearby factory involved in the production of veterinary prophylactic drugs, including vaccines against anthrax. Unfortunately despite sealing off the toxic waste storage facility with concrete, which provides isolation from the surrounding environment, the factory does not have any resources for the radical disinfection of the waste.
- during the decade 1994-2004, none of the 515 anthrax sites in the Vologodskaya oblast has shown disease activity.
- Ukraine : from 2000 through 2004, there were 26 bovine anthrax outbreak with some 141 animals affected, 3 sheep/goat outbreaks reported (in these species, un-reporting is the norm) with 13 deaths, 2 equine outbreaks with 7 deaths, and 5 pig outbreaks and only 5 deaths reported. The give-away is that in the same period, there have been 15 human cases reported
- Georgia has a severe anthrax problem in its livestock. The diseaseis regularly seen in a number of areas, and the government is struggling to develop an efficient, and effective, veterinary control program. Human cases have been regularly reported since 1995: 33 cases in 1996, 4 cases in 1997, 11 cases in 1998, 51 cases in 1999, 21 cases in 2000, and 26 cases in 2001. This is not the 1st time urban cases in Tblisi have been only the tip of a rural epidemiological anthrax iceberg. Gardabani district is regularly blamed, but it suffers from being close to Tblisi, and, consequently, is reported upon in the press. Some of the 2001 cases were in Abkhazia, Zugdidi district.
- Europe
- Finland : outbreaks in 1988 and in 2004 (southern Finland)
- Italy. Basilicata : this mountainous area normally has 2 to 3 outbreaks each summer. This series of outbreaks has been ascribed to the heavy rains eroding historically contaminated cattle graves and thus depositing spores in the pastures. In 2004 the 1st outbreak was noted in late July 2004 and in retrospect was probably just the usual summer incident. But in late August this epidemic started, and by 24 Sep 2004 totalled some 36 known outbreaks; in this hilly area, there are certainly other cases not observed or not reported. The total recorded cases are 54 cattle, 7 horses, 11 sheep, and 4 red deer. Presumably there have been subsequent outbreaks in the region. 2 veterinarians have developed cutaneous anthraxref.
- UK : 2 cows died of anthrax on a beef farm in Rhondda Cynon Taff in south Wales on Apr 2006. It is the 1st case in Britain since 2002, when a cow died at a farm in Wrexham, considered to be a sporadic incident on a farm which had 3 anthrax cases in the previous 2 decades. There was also a case in cattle in Clwyd in 1992 and pigs were confirmed
- Africa :
- Zambia : in this part of Africa it is not unusual to see a ratio of 10 human cases per bovine case
- Zimbabwe : just over 20 years ago it had 10 000 human cases when disease control had been significantly weakened by their civil war. With the ongoing lawlessness and fragile infrastructure, this may become a repeat of those events. The first cases of anthrax at Morgenster in Masvingo were reported in September 2003, and so far Bikita has the highest number, with 147 cases having been reported in Ngorima, Mutikizizi, and Devure. In Gutu district, a total of 82 cases, including 2 deaths, were reported, while in Chivi 51 cases and deaths were reported. It is highly probable that the true incidence of human cases in rural areas is already a multiple of the reported number. In normal circumstances this would have been controlled and prevented from the start by proper livestock vaccination.
- Asia :
- India : anthrax is not frequent in western India but not unknown. It is most common in the south and through the eastern states. The Indian National Survey for 1989-94 had southern India and Tamil Nadu with the highest incidences for the disease. A companion document for 1991-1996 had it occurring in Tamil Nadu each year in cattle, buffalo, sheep, and goats in sometimes spectacular numbers. In 1996 a paper described some 29 patients with anthrax meningitis with an unfortunately high lethalityref. A longer version can be found in the Indian Journal of Medical Microbiologyref, 1996, 14:63-67, with maps showing where cases have been seen in the state, including a spot-map of human and animal cases in the North Arcot Ambedkar district. In 2003 a paper described 27 patients seen at the Christian Medical College & Hospital, Velloreref, so I think we can unfortunately assume that the disease continues both in humans and the rural livestock in Tamil Nadu, much as before
- USA : the last official update/newsletter was from 28 Jul 2005. The 16 Aug 2005 map has the following numbers of outbreaks in the following 11 South Dakota counties: Brown (4), Day (1), Dewey (7), Hand (2), Hughes (2), Hyde (2), Marshall (3), Potter (7), Spink (2), Sully (9), and Walworth (1), which sum to 39 outbreaks. But the map, for some reason, is titled "2004-2005 Anthrax Cases in South Dakota." It would seem that the cases in northeast South Dakota may be epidemiologically linked to the cases in southeast North Dakota, where the weight of the latter state's outbreaks are. North Dakota Department of Agriculture anthrax map. As of 16 Aug 2005, North Dakota has had 86 cases (premises) in 13 counties. The cattle trails project was to verify the traditional belief that anthrax was related to the cattle trails of the 19th century. If your ranch/farm was in a county within some 10 km of a cattle trail going from the south to the north, there was a significant risk, approx. 10 percent, of historical anthrax in that county. This did not apply to the emigrant trails from east to west. This made sense, as the south-to-north trails, including those from Texas to California, involved longhorn cattle moving from an historic enzootic region of southern Texas and Louisiana. The east-west trails involved less cattle and these were largely British breeds, mainly Herefords, from breeding areas without anthrax. The Red River trails were to get people, goods, and livestock from St. Paul up into northwestern Minnesota and on to southern Manitoba and Winnipeg.
- Peru : bovine anthrax is reported annually in and occurs in about 5 out of 10 of the coastal departments. Lately, it has been reported in the following departments: Ancash, Cajamarca, Huanuco, Ica, La Libertad, Lima, Moquegua, and Tumbes.
- if possible, carcasses should be burnt. But this can present serious problems when there is a lack of firewood and staff. Hippos and elephants are fuel-hungry species. If all else fails, the best option is to stop scavengers opening up carcasses for the first 3 or 4 days so that the carcass can ferment and the pH drops to acid levels, thereby killing the vegetative cells. Without oxygen they cannot sporulate. In this way the environmental contamination is minimal, even if the carcass is later opened and the bones fed on and dragged around. And even with sites that have spores, repeated sampling over the years has shown some sites becoming 'apathogenic' from plasmid loss. Examination of such sites is needed, if only to rule out those that present no risk. Watery diarrhea is not a normal sign of clinical anthrax, which is normally characterised by peracute death in cattle. Bloody exudates from the various orifices post-mortem, though common in textbooks, in reality is not a consistent feature of livestock anthrax. The US Navy test kit depends on the PA titre in the bloody fluids, and this titre falls off with time such that carcasses over 3 days old can be negative though culture-positive. For fresh cases it is unbeatable.
- Carbosap vaccine (2 injections). Normally anthrax is rarely seen in commercial herds in Africa because of the higher level of management practiced and regular vaccinations. If animals are not in good condition when vaccinated, any immunity developed is been minimal. Anthrax is not a contagious disease. Post-outbreak herd quarantine is to stop animals leaving the farm that are incubating the disease and before the vaccine protection has kicked in. With Sterne it is frankly rare to see deaths from anthrax > 8 days after vaccination; normal development of immunity is faster. The most efficient way to control anthrax in cattle herds is (1) to properly and quickly deal with the affected carcasses; (2) to treat the survivors with a long-acting antibiotic (such as LA200, but use normal penicillin with horses, as LA200 is painful); and (3) to wait 7-10 days before vaccinating with Sterne or another recognised live vaccine.
- Sterne vaccine : the common experience is that you will get deaths up to 8 days post-vaccination because it is only at that point that protection has been fully developed. And because of that 8-day risk window, ranchers are encouraged to 1st treat their stock with long-acting antibiotics to treat any apparently healthy animals that are incubating an infection. LA200 gives a 3-day cover but cannot be used with lactating dairy cows. Benzathine Penicillin with Penicillin G Procaine gives a 48-hour cover and can be used with dairy cows. Because the latter is shorter acting, it may not be as efficacious and may need to be given twice or in larger doses than specified on the bottle. Anyway, if there have been deaths in a dairy herd, animals' temperatures should be checked morning and afternoon when they come in for milking until the vaccination has taken effect; any animal with a temperature or seeming to be ill (dairymen know their animals) should be taken out of the line and treated. There is no risk to humans from the vaccine when they drink the milk from healthy vaccinated cows. If you use the antibiotics after the vaccine, it can stop the vaccine from developing a full immunity by killing circulating live vaccine organisms. So the best course of action is to 1st treat with antibiotics, wait 7-10 days, and then vaccinate. If you use antibiotics simultaneously with vaccine, you will have to revaccinate the animals 2 weeks later to get any long term protection. Once a herd has had anthrax, you should revaccinate each following spring for at least 3 years because of any pasture contamination. This also applies to ranchers who may not have had any anthrax deaths but whose neighbors have. You cannot count on the latter remembering to revaccinate next year, and when they are reminded by cows dying, it may be too late for you to protect your animals. I have seen this happen more than a few times.
- simultaneous treatment with antibiotics and Sterne only results in killing the live vaccine and any incubating infections without any medium-term benefits. The report of human cases from consuming "preserved meat" follows from the need of farm managers -- usually poor relatives of the farm owner -- having to prove that any missing animals had died and had not been sold or given away. Thus animals dying are skinned; the meat is stripped from the carcass and sun-dried; and the head, hide and dried meat are available to the owner when he or she later visits the farm. This handling maximises the number of spores in these products)
- the animal which introduced the infection may no longer be alive;
- although the disease reached and became established in the herd in Cornwall, it may not have persisted elsewhere.
- 1) bovine brucellosis or any suspicion thereof is notifiable;
- 2) the entire cattle population is under official veterinary control and it has been ascertained that the rate of brucellosis infection does not exceed 0.2% of the cattle herds in the country or zone under consideration;
- 3) the serological tests for bovine brucellosis are periodically conducted in each herd, with or without the ring test;
- 4) no animal has been vaccinated against bovine brucellosis for at least the past 3 years;
- 5) all reactors are slaughtered;
- 6) animals introduced into a free country or zone shall only come from herds officially free from bovine brucellosis or from herds free from bovine brucellosis. This condition may be waived for animals which have not been vaccinated and which, prior to entry into the herd, were isolated and were subjected to the serological tests for bovine brucellosis with negative results on 2 occasions, with an interval of 30 days between each test. These tests are not considered valid in female animals which have calved during the past 14 days. In a country where all herds of cattle have qualified as officially free from bovine brucellosis and where no reactor has been found for the past 5 years, the system for further control may be decided by the country concerned)
- Europe
- Great Britain : > 8 millions animals (around 1 in 8 were cows) were slaughtered in 2001 in a desperate effort to control the most serious British epidemic of FMD disease in over 30 years, caused by serotype O. Inactivated vaccine, which had proven to be successful for the eradication of the disease, was ruled out because the blood of dosed and infected animals is indistinguishable (their immune responses are similar) and symptoms can take days to develop : during this delay a healthy-looking animal can spread the FMD virus, so under current European and American laws vaccinated animals cannot be bought or sold due to inability to distinguish vaccinated animals from infected one. The European Commission in 1990-1, after undertaking a cost benefit analysis, implemented a policy of non-vaccination to increase export opportunities and to ensure high animal health standards : this outbreak containment policy requires an export ban on all livestock and animal products from any affected country, along with movement restrictions and the slaughter and burning of all cloven-hoofed animals that are either infected, on infected premises, or in contact with infected animals. Until now the European Union has remained free of FMD since an outbreak in Greece in 1996. At the time, authorities were criticised for their lack of preparedness. Several years on, the government has taken important steps to avert a future outbreak, summarized in a report (alternative URL) by the Royal Society : first, the government has taken steps to prevent the disease entering the country by clamping down on imported meat and animal feed that might harbour the virus. Second, it has made moves to stop a small outbreak escalating into a full-scale epidemic by, for example, making faster diagnoses and introducing measures to freeze movement of infected animals immediately. But on the down side, the panel concludes that the government is not fully prepared to thwart the disease by vaccinating animals. Vaccination was not used in the 2001 British epidemic, partly because it is difficult to tell animals that have been vaccinated from those that have been infected, as both produce a similar immune response. Tests to distinguish vaccinated and infected animals have now become available and vaccination is considered a first line of defence, but the tests have not yet been validated and so are not ready to use. The country also lacks the infrastructure to ensure that vaccines and tests could be deployed on a massive scale, and there is no clear commitment to use it widely. The report urges the government to re-visit its emergency plans every few years to ensure that these remain adequate as farming practices change. The government has already taken steps to identify remaining shortfalls in its foot-and-mouth strategy. Exercise Hornbeam, for example, simulated days 7 and 8 of a disease outbreak in June 2004. There is an urgent need for a vaccine that can prevent the disease from taking root in animals in the first place rather than simply protecting them from the symptoms of the disease
- South America : during 2003, FMD was officially reported from 3 countries: Argentina, Bolivia, and Paraguay. Serotype C has been reported in the Brazilian state of Amazonas, in the North of Brazil in 2004 after last detection in 1995 : the Argentine vaccine is bivalent, O and A, tetravalent in serotype, and contains, besides O, the antigens A-24, A-2000, and A-2004, but it does not contain type C. The Reference Lab at the Institute for Animal Health, Pirbright does not show any isolates of Type C after 1996. During this period, most of the outbreaks in South America were either Type A, Type O, or a mixture of both types.
- Asia : 2 FMD serotypes are, reportedly, evolving now in eastern Asia/the far east: type Asia 1 in Russia's Amur region (Khabarovsk province); type A in eastern Mongolia's Dornod province. They are > 1000 miles apart; both share borders with the People's Republic of China
- between 1990 and 1996, there were 29 reports of type C virus, almost all from Asia. Nepal led the list with 14 isolates, Philippines was next with 8 isolates, and one came from the Soviet Union (1991). The data obviously indicate that Type C has been absent from the world scene for several years now. It is very important to figure out exactly how it came back and to ensure that it is contained on the island in the Amazon. FMD is endemic in Cambodia : according to Cambodia's detailed monthly reports to the OIE, FMD was recorded there during each month of 2003 (20 outbreaks), affecting 3023 cows, 528 buffalo, and 351 pigs in 8 provinces (The cattle population of Cambodia is approximately 2.9 million; buffalo, 0.6 million; and pigs 2.1 million) and the last FMD virus typing of samples from Cambodia was carried out at the World Reference Laboratory (Pirbright, UK) in 2000 (serotype O was identified). FMD is endemic in Pakistan, reportedly caused, during 2003, by 3 serotypes: A, Asia1, and O. FMD has been spreading in Zambia since February 2004.
- Russia's concern about the FMD situation in China is understandable in view of the outbreak in dairy cattle, caused by FMD virus serotype O of the pan-Asian group, detected in Amur, 15 km from the Chinese border, in April 2004. China's last OIE-reported outbreak of FMD occurred in May 1999. It was caused by FMD serotype O (most probably of the pan-Asian group). Totally, 8 outbreaks were officially reported: 5 outbreaks from Tibet, 2 from Hainan, and one from Fujian. The disease was reported as absent during 2000-2002ref. During 2003, 4 China's monthly reports are available on OIE's Handistatus database and cover only the period September - December, and stated that the disease was absent. In 2004, monthly reports cover the period January - August 2004, also stating absence of the disease. No later reports are available. An OIE experts mission visited China during 10-19 May 2004. According to the Mission's 20-page report (which was available on OIE's web-site until very recently), 6 Reference Laboratories for the following List A diseases were visited and reviewed: classical swine fever (CSF), rinderpest, avian influenza (AI), contagious bovine pleuropneumonia (CBPP), Newcastle disease (ND) and bovine spongiform encephalopathy (BSE). Hopefully, FMD will be covered in future visits. In 2004 Russia suffered an outbreak of FMD, serotype O, in dairy cattle in the Amur region, 15 km from the Chinese border. Subsequently (in September 2004), Russia restricted imports from China. The 2 official reports of Russia to the OIE on the 2004 outbreak mentioned a total number of 141 dairy cows (12 months old) exposed to the virus, which was identified as serotype O of the pan-Asian group. 87 of them were clinically affected; 890 animals -- including in-contact animals -- were destroyed. The current media-derived data concerning 2004's outbreak are somewhat different, particularly in regard to the alleged involvement of pigs. Clarifications will help. As to the current outbreak, caused by a different serotype (Asia 1), here also there are discrepancies between official and unofficial data, particularly regarding the numbers of affected animals. The 2 affected bovines mentioned in the official notification might reflect the number of sampled animals tested in the laboratory. It will be helpful to obtain the number of exposed and clinically affected animals, and to exclude -- or otherwise -- the possibility that pigs are involved as well. The event in Busse, Svobodnenskiy, Amur region (Amurskaya oblast) (20 km from the closest village in the Russian territory and 300 m from the border with the People's Republic of China) started on 6 Jun 2005 and involved 2 cases. The Asia 1 epizootic in Russia's far east seems to continue its pace; a look at the map will reveal that this is not necessarily a spread within Russian territory, but more probably repeated introductions from neighboring China. Busse, where the 1st outbreak was reported in June 2005, is situated on the Amur river, which separates Russia from China. The 3 villages in the Khabarovsk region, found infected in August 2005, are situated on the Ussuri river, also separating Russia from China. This area is more than 1000 km distant (southeast) from Busse. The new outbreak, reported on 26 Aug 2005 in the Primorskiy region, also borders China, about 700 km south of the foci in Khabarovsk. According to an analysis by the FAO (June 2005, following the Amur outbreak), countries bordering China to the south and east could be considered at risk of Asia 1 on a geographical basis. Indeed, outbreaks have been recorded in Mongolia and Myanmar. Unless drastic and efficient control activities are immediately applied in China, additional introductions of the virus to other countries might be expected along her borders. The further spread, observed since June 2005, prescribes the need for increased alertness in the region, including consideration of the need to apply mass vaccinations against serotype Asia 1.
- Pakistan : FMD is endemic; the efficient way to help the farmers reduce their losses is a preventive, not a curative one. Pakistan's last available annual report to the OIE, for 2003, does not include data on vaccinations. In 2002, 13 690 bovines and 28 765 buffalo were reportedly vaccinated; the national herd included 22.8 million bovines and 24 million buffalo. During 2004, 8 samples were sent from Pakistan to the OIE/FAO World Reference Laboratory for Foot and Mouth Disease at Pirbright, UK. 2 of them were found positive for FMDV (serotype Asia 1). During 2003, 81 samples were sent, of which 29 were found positive for FMDV serotype O, 8 serotype A and 4 serotype Asia 1. In 2 samples, mixed infections, including serotypes O and A, were demonstrated
- China : according to China's reports to the OIE, not a single outbreak of FMD was recorded there between May 1999 and the end of 2004. Since 13 May 2005 to 13 July 2006, China has sent the OIE 14 official notifications on FMD in bovines, caused by FMD virus serotype Asia 1, in the following 9 provinces (in chronological order of their 1st recordings): Jiangsu, Beijing, Hebei, Xinjiang, Gansu, Qinghai, Shandong, Ningxia and Jiangxi. During 2005, the Chinese veterinary services sent the OIE 6 reports on FMD, serotype Asia 1, causing 10 outbreaks in 4 (out of China's 22) provinces, 1 out of China's 5 autonomous regions and 1 out of China's 4 major municipalities. The affected provinces were (in brackets, number of outbreaks): Shandong (2), Gansu (1), Qinghai (1), Hebei (2), Xinjiang Uygur Autonomous Region (2), Beijing municipality (1), and Jiangsu (1). They spread over distances of about 4000 km, from the far eastern parts of China (Jiangsu, Shandong, Hebei and Beijing) to the centre (Gansu), midwest (Qinghai) and the far north west (Xinjiang autonomous region), as follows:
- 1. 13 May 2005 / bov / Jiangsu province (east)
- 2. 13 May 2005 / bov / Shandong province (east)
- 3. 26 May 2005 / bov / Xinjiang (autonomous region, north-west)
- 4. 26 May 2005 / bov / Hebei province (east)
- 5. 26 May 2005 / bov / Beijing municipality (east)
- 6. 20 Jun 2005 / bov / Xinjiang (autonomous region, north-west)
- 7. 27 Jun 2005 / bov / Hebei (east)
- 8. 20 Jul 2005 / bov / Qinghai (mid-west)
- 9. 20 Jul 2005 / bov / Gansu (centre/mid-west)
- Cambodia : in 2000, when serotype O was identified. An outbreak in pigs occurred in 2005
- Peninsular Malaysia reported 39 outbreaks in 1996, 39 in 1997, 10 in 1998, 9 in 1999, 3 in 2000, 189 in 2001, 39 in 2002 (incomplete outbreak number but some 5760 individuals were affected), 21 in 2003, 37 in 2004, and only 1 in 2005
- Kyrgyzstan (officially, Kyrgyz Republic; 2005 est. pop. 5 146 000; c. 76 600 sq mi or 198 400 sq km), borders China in the southeast, Kazakhstan in the north, Uzbekistan in the west, and Tajikistan in the southwestref. The 2005 numbers of FMD-susceptible species, according to FAO statistics, are the following: cattle 1 034 890, sheep 2 965 220, goats 808 397, pigs 82 659. FMD outbreaks were last reported from Kyrgyzstan by ProMED-mail in January 2004. However, according to Kyrgyzstan's official reports to the OIE (their last available report covered 2004), no outbreaks were officially recorded after Feb 2001, when 2 outbreaks were reported in Naryn and one in Issyk-Koul. They were reportedly caused by FMD virus serotype Oref
- Recent serotyping of samples sent from Southeast Asian countries to Pirbright reveals the presence of serotypes O (Viet Nam, Myanmar, Hong Kong and Thailand), A (Thailand) and Asia 1 (Hong Kong). The spread of serotype Asia 1 throughout China has been recently reported, with one penetration into Russia (Amur).
- Turkey : since 21 Jan 2006 outbreak due to virus type A was reported in the village of Nadirli (Babaeski, province of Kirklareli), in Thrace region. According to the OIE, the last reported outbreak was in 2001; FMD serotypes A and O are endemic in Turkey, excluding Thrace, which has been free for years. An FMD outbreak occurred in Georgia in 2002. An extensive outbreak of FMD occurred in the region in 1996 affecting Bulgaria, Albania and several parts of the former Yugoslaviaref
- Africa
- Zambia : according to current OIE's epidemiological statistics, FMD types SAT1, SAT2, and SAT3 have been officially reported from northern province in each of the months Feb-Jun 2004. FMD type SAT1 was reported during July in the central province and in Sep 2004 in an unspecified arearef. Final data for 2004 and an update for the 1st semester of 2005, from all member countries including Zambia, might be expected during the current General Session of the OIE in Paris (22-27 May 2005). Dipping cattle has no impact upon the control of FMD; however, it is an important measure for the control of corridor disease.
- Botswana : according to 2003 report, following the 2002/2003 FMD outbreaks, 358 088 head of cattle were vaccinated -- all within the "vaccination zone". The vaccine is produced by the Botswana Vaccine Institute, which is OIE's Regional Reference Laboratory for FMD, Africa. A National Animal Health Status Report for 2004, submitted by Botswana for the 16th Conference of the OIE Regional Commission for Africa in Khartoum (Sudan), 7-10 Feb 2005, included the following FMD-related data pertaining to the recent epidemiological situation: "FMDV in Botswana is restricted to the northern part of the country where the 3 South African Territory serotypes (SAT I, II and III) are maintained within the African Buffalo (Syncerus caffer) populations. Before the 2002/2003 outbreaks, Botswana had been free from FMD for over 21 years. FMD control in Botswana is based on vaccination of cattle and movement control of cloven-hoofed animals and animal products. To that end, a system of zoning using disease control cordon fences has been employed. The 2002/2003 FMD outbreaks were successfully controlled through stamping out. Currently The World Animal Health Organisation (OIE) recognizes Botswana as having zonal freedom from FMD without vaccination".ref
- New Zealand : a letter claimed a release on Waiheke Island (39 farmers) on 9 May and threatening a further release unless the government responded to demands for taxation changes, and paid a large sum of money. The New Zealand police are investigating the attempted extortion and are treating the letter as a hoaxref1, ref2. All stock will be checked every 48 hours for 14 days -- the longest possible incubation period for FMD before clinical symptoms appear. Pigs are by far the greatest risk of spread, but there are few pigs on Waiheke Island. Cattle and sheep are a much lower risk -- there are some 2500 cattle and 18 000 sheep on the island. FMD is an unwanted organism under the Biosecurity Act of 1993. Anyone convicted of spreading it faces a penalty of up to 5 years' imprisonment or a fine up to $100 000 [USD 73 000]. Under the Crimes Act anyone convicted of threatening to commit a crime that would cause major damage to the economy can be sentenced to 7 years in jail. Section 298A stipulates that anyone causing disease or sickness to animals can be sentenced to up to 10 years in jail. A 2nd letter, received 16 May 2005 by Wellington's Dominion Post newspaper, has stated that the claims made last week are a hoax and that no FMDV was released in New Zealand. As a result of this additional information and the surveillance results thus far, MAF now intends to remove the legal restrictions covering the movement of animals and risk goods off Waiheke Island by 5 p.m. on Tue 17 May 2005. MAF will, however, continue with a low level of monitoring of livestock on the island until 23 May 2005
- early to mid-1960s outbreak of FMD a few miles from the Animal Virus Research Institute at Pirbright, UK, in a ?dairy herd, when the former was doing experiments on birds possibly transmitting virus and the infected animals were in a loose box (stable) one side of an open courtyard, and target animals on the opposite side
- the other was from an offshore Danish FMD research institute that affected a herd some kilometers away in Norway, about the same time. Present institutional construction has dealt with any such risks today.
- milk
-
Mycobacterium bovis
: 15.8% of cattle in Devon, UK has been hit by an outbreak of bovine
tuberculosis (BTB), with 537 new outbreaks in 2003, more than 5 years
into the Krebs culling trials of badgers, which are seen as the main carrier
of the disease. Eradication of bovine TB reduces disease and death from
tuberculosis among farmers and people in contact with infected cattle,
or who drink unpasteurized milk. Bovine TB had spread to deer, yellow-necked
mouse, wood mouse, shrew, polecat, muntjac and stoatref.
- pearl disease : bovine tuberculosis of the peritoneum and mesentery in which the tubercles are calcified and pearllike
-
Mycobacterium
avium subsp. paratuberculosis
(Johne's disease / chronic dysentery of
cattle / paratuberculosis : a usually fatal form of chronic distal
enteritis or proctitis,
affecting chiefly cattle but also ruminants (including Oryctolagus
cuniculus, Ovis
aries, Lama
pacos and Capra hircus)
and other animals. It remotely resembles a tuberculous infection, and is
marked by lymphangitis
or mesenteric lymphadenitis,
intermittent or persistent diarrhea, progressive emaciation, anemia, and
extreme weakness. MAP can live undetected in cattle for years. Infected
cows secrete the bacteria into their milk and on to their pastures)
-
cowpox virus
-
pseudocowpox virus / paravaccinia
virus / milker's nodule virus (MNV)
-
Russian
Spring-Summer encephalitis virus (RRSEV)
- the 2002 NAHM's Dairy Survey indicated that 87.2% of dairy farms in the United States feed waste milk to their neonatal calves. Although cost-effective, this practice can lead to increased calf morbidity and mortality due to ingestion of pathogenic agents. In an effort to reduce the risk of infection, dairy producers are implementing on-farm pasteurization of the waste milk as a control procedure before feeding the milk to calves. In the present study, the efficacy of a commercial high-temperature, short-time (HTST) on-farm pasteurizer unit to destroy MAP, Salmonella enterica spp., and Mycoplasma spp. in raw milk was evaluated. Replicate experiments were run for 3 isolates of M. paratuberculosis, 3 serovars of Salmonella (derby, dublin, typhimurium); and 4 species of Mycoplasma (bovis, californicum, canadense, serogroup 7) at 2 different levels of experimental inoculation. In addition, HTST pasteurization experiments were performed on colostrum experimentally inoculated with MAP. After culture of the pasteurized milk samples, no viable MAP, Salmonella, or Mycoplasma were recovered, regardless of species, strain, or isolate. Pasteurization of colostrum was also effective in the destruction of MAP but resulted in an average 25% reduction in colostral immunoglobulin. These results suggest that HTST pasteurization is effective in generating a safer product to feed to young calvesref.
- CNS :
-
PrPSc
=> bovine spongiform encephalopathy
(BSE) / mad-cow disease is a TSE.
The first clinical case occurred to cow 142 from Pitsham Farm in Sussex
on December 22, 1984 but the existence of a new disease was first confirmed
microscopically in November 1986. It was not, however, until June 1987
that the Consultant Pathology Unit at the Central Veterinary Laboratory,
Weybridge, UK, confirmed this as a case of BSE. However, the BSE inquiry
("Lord Phillips Report", October 2000) further remarked that Epidemiological
evidence given to the Inquiry suggests that it is likely that the first
cases of BSE probably originated early in the 1970s - possibly a single
cow or other animal that developed the disease as a consequence of a gene
mutation
- infection is acquired by some animals between age 3 and 5 by eating ruminant-derived processed animal proteins (PAPs) including meat and bone meal (MBM) : 2.5-6 years of incubation => circling. At least 3 oral challenge trials are being performed in various countriesref1, ref2 :
- in DEFRA's research project SE1736 (1998-2004), groups of calves were challenged orally with either 100g or 1g of BSE infected bovine CNS of known infectious titre. Tissues and fluids were also produced from age matched controls kept under similar husbandry conditions. In the 100g challenge group, a wide range of tissue and fluid samples were collected at 3 month intervals from 30 months post-challenge. In the 1g challenge group, a wide range of tissues and fluids were collected at approximately 6 month intervals from 36 months post-challenge. The tissues and fluids from these animals have been collected following strict protocols and are archived under ISO9001 conditions. The TSE archive of the Veterinary Laboratories Agency (VLA) represents a valuable resource of bovine BSE materials, which is used within the UK program and may be supplied to those engaged elsewhere in BSE research, particularly, but not exclusively, for the development of diagnostic tests. As this is a limited and valuable long term resource, the approval of requests, and release of material, is through an independent archive advisory group (IAAG) made up of scientists with TSE research experience. IAAG consists of 6 researchers from the UK, France and Germany and provides an external review to ensure all requests are dealt with fairly. Officials from Defra, the Food Standards Agency and the European Commission oversee the group
- another trial is led by a special BSE infection unit of the Institute of Novel and Emerging Infective Agents (INNT) at the Federal Research Centre for Virus Diseases of Animals (BFAV) on the Island of Riems (a tiny island in the Baltic sea). In this study, begun in early 2003, 56 calves were orally challenged (100g brain stem homogenate each, 1st group (28 animals) in Jan 2003, 2nd group (28 animals brought to the Island of Riems after 6 weeks and quarantined for further 4 weeks) in May 2003). Another 18 calves serve as controls. Blood (serum, plasma etc.), CSF, and urine samples regularly (2 to 4 samples per month) are collected, and selected animals are serially killed and autopsied. From each animal, a panel of more than 120 tissue and bodily fluid samples are taken and preserved in a number of ways (frozen, snap-frozen, formalin-fixed etc.). All samples are taken under BSE-sterile conditions. Samples considered to be important in terms of BSE pathogenesis, and consumer safety, are used in a bioassay experiment utilizing bovine PrPC over-expressing transgenic mice, which are lacking a species barrier for cattle BSE infectivity. British scientists have supported this infection trial in providing > 5 kg brain tissue from BSE cattle. The study aims to research the course of infection from the start of the infection until the outbreak of the disease. During the 1st year of this trial, 9 out of the 56 challenged calves have been sacrificed and 38 000 specimens collectedref. As of May 2004, > 60 000 samples have been collected from the animals of the German BSE pathogenesis study, and > 200 000 samples will have been taken by the end of the experiment in the year 2007ref. > 4000 samples have already been distributed to German TSE research groups and commercial test developers. This experiment is a German initiative within the framework of the German TSE research platform. The distribution of the samples is regulated by the TSE-platform's advisory board, which is composed of elected members -- German TSE researchers -- as well as the heads of the German CJD and BSE archives.
- tallow-based calf milk-replacer (CMR) associated with the allowable levels of impurities in tallowref. Interestingly, EU's Scientific Steering Committee has not classified cattle tallow derivatives as "not infectious"
- transplacental transmission may occur
- 10-fold concentrated urinary proteins from scrapie-infected mice with lymphocytic nephritis induced scrapie upon inoculation into 50% of noninfected indicator mice. Prionuria was found in presymptomatic scrapie-infected and in sick mice, whereas neither prionuria nor urinary PrPSc was detectable in prion-infected wild-type or PrPC-overexpressing mice, or in nephritic mice inoculated with noninfectious brain. Thus, urine may provide a vector for horizontal prion transmission, and inflammation of excretory organs may influence prion spread The research may explain how animals such as sheep, elk and deer transmit prion diseases. In the USA, a chronic wasting disease is spreading like wildfire among elk and deer. About 20% of the wild deer in some parts of Colorado are infected, and yet these animals are herbivores. Nobody understands what controls the spread : dust mites have been suggested as one method of transmission. Animals may be eating urine-contaminated grass. An explanation that involves urine has difficulties however : the concentration of prions found in the mouse urine in the experiment was 10,000 times lower than in the lymphatic organs, and a million times less than in the brains, the original site of infection. The risk of getting sick by touching or ingesting infected urine is minuscule. Quite apart from the low concentration of prions in urine, it would take a higher dose of the proteins to cause infection this way than through injection into the brain. As yet, there are no data on the risk that might be attached to contact with urine from vCJD patients. On the other hand, nobody wants human prions in the hospital laundryref
- proteins
- meat meal is seldom produced as per definition anymore, but when used was in pet food as applicable.
- meat and bone meal (MBM) can generally be made from raw material of all livestock species. Obviously with the current feed rule, if the product contains raw materials originating from ruminants, it cannot be fed to cattle or other ruminants. MBM could be made from pure bovine, porcine tissues, etc. and traded as such. This may include blood meal, spray-dried animal blood, poultry meal, poultry byproduct meal, poultry hatchery byproducts, and blood protein. MBM is allowed to be in pet food. However, the pet food industry does not want downer animals in its products, and is actively working to institute a similar ban.
- fats : tallow, lard, gelatin, greases (yellow and white), fatty acids, glycerine, etc. can be used in the human food chain. So the key for use of rendered products in the human food chain (lard, tallow, gelatin) must be inspection by the Food Safety nspection Service (FSIS). They are products that have scientifically been shown not to harbor prions.
- fish meal and bakery byproduct meals (those damaged packages of Twinkies, potato chips, corn chips, and other similar products that are crushed and recooked to make a pleasant grain-based product that may be fed to some pets). Their uses include livestock and poultry feeds; pet foods; industrial uses such as lubricants, paints, ipsticks, gums, glues, etc. None of the bakery by-products goes into the human food chain. Blood meal has not been shown to process the prion agent. However, it is used by gardeners.
- is there a risk that the BSE-agent was imported into the country under consideration ("external challenge")?
- if the BSE-agent was introduced into a country, would it have been recycled and amplified ("unstable" situation) or was the BSE/cattle system of that country able to eliminate the agent ("stable" situation)?
- level I (highly unlikely) : Argentina, Australia, Botswana, Brazil, Chile, El Salvador, Iceland, Namibia, New Caledonia, New Zealand, Nicaragua, Panama, Paraguay, Singapore, Swaziland, Uruguay, Vanuatu
- level II (unlikely but not excluded) : Colombia, Costa Rica, India, Kenya, Mauritius, Nigeria, Norway, Pakistan, Sweden
- level III (likely but not confirmed or confirmed, at a lower level) : Albania, Andorra, Austria, Belarus, Belgium, Bulgaria, Canada, Croatia, Cyprus, Czech Republic, Denmark, Estonia, Finland, France, Germany, Greece, Hungary, Ireland (Eire), Israel, Italy, Japan, Latvia, Lithuania, Luxembourg, Macedonia (FYR), Malta, Mexico, Netherlands, Poland, Romania, San Marino, Slovak Republic, Slovenia, South Africa, Spain, Switzerland, Turkey, USA
- level 4 (confirmed, at a higher level) : Portugal, UK
- UK is classified in the highest (GBR IV) EU risk category group. > 95% of BSE cases were detected before 2000 : incidence peak occurred in 1992 (37 000, 700 new cases per week) and is currently declining by some 40% year-on-year : 184 138 cows have died from BSE since 1987 (1443 (270.56 per million bovines aged over 24 months) in 2000, 1202 (232.76 per million bovines aged over 24 months) in 2001, 1144 in 2002 (445 clinical cases and 594 cases detected by tests; 228.24 per million bovines aged over 24 months), 611 (122.44 per million bovines aged over 24 months) in 2003, 343 (67.796 per million bovines aged over 24 months) in 2004, 151 in 2005. There are estimated to have been 4 million BSE infected cows compared with 184 131 officially reported cases
- Portugal is classified in the highest (GBR IV) EU risk category group : 949 cases since 1987 (186.95 indigenous cases per million bovines aged over 24 months; 110 cases (137.88 per million bovines aged over 24 months) in 2001; 86 (107.80 per million bovines aged over 24 months) in 2002; 133 (137.19 per million bovines aged over 24 months) in 2003; 91 in 2004 (93.870 per million bovines aged over 24 months); 13 at 22 Apr 2005)
- Ireland : 1470 cases since 1987 (38.17 per million bovines aged over 24 months in 2000 (annual incidence rate in cases detected by the active surveillance programme = 17.93; annual incidence rate in BSE clinical cases = 35.356, 246 (61.80 per million bovines aged over 24 months; annual incidence rate in cases detected by the active surveillance programme = 29.90; annual incidence rate in BSE clinical cases = 30.90) in 2001; 333 (88.39 per million bovines aged over 24 months) in 2002; 183 (57.81 per million bovines aged over 24 months) in 2003, 117 (43.327 per million bovines aged over 24 months) in 2004, 23 at 22 Apr 2005). According to official Irish statistics, the percentage of cases diagnosed in animals less than 6 years of age has declined from 40% in 2000 to 16% in 2001, 2% in 2002, and 0% in 2003.
- Spain : 532 cases since 1987 ((0.59 per million bovines aged over 24 months), 82 in 2001 (24.23 per million bovines aged over 24 months), 127 in 2002 (37.95 per million bovines aged over 24 months); 167 in 2003 (46.31 per million bovines aged over 24 months), 137 in 2004 (38.945 per million bovines aged over 24 months), 12 at 22 Apr 2005). It is the only European country not showing, in 2003, a decline in the number of diagnosed cases
- Switzerland : 456 cases since November 1990 ((40.6 per million bovines aged over 24 months); 42 (49.1 per million bovines aged over 24 months) in 2001; 24 (27.93 per million bovines aged over 24 months) in 2002; 21 (24.86 per million bovines aged over 24 months) in 2003; 3 (including a case in a zoo zebu) in 2004 (3.750 per million bovines aged over 24 months); 0 at 22 Apr 2005). Switzerland reported in November 1990 the first BSE case on the European mainland which could not be attributed to an animal imported from Great Britain. According to the official Swiss data, the infection was presumably due to feed constituents that had been inadequately heated; material which originated from Britain was most probably given new origin labelling and then imported via an indirect route, as according to the Swiss foreign trade statistics, only very small quantities of meat-and-bone meal were imported directly from Great Britain. Switzerland was the first country to introduce active monitoring of BSE, in 1999; the Swiss prionic BSE test is used for the systematic testing of groups of cows at risk. The annual BSE incidence rate (number of indigenous cases per million bovines aged over 24 months) during the years 1999-2003 was 58.7, 40.6, 49.1, 27.93, and 24.86, respectively
- Belgium : 127 cases since 1987 (5.53 per million bovines aged over 24 months in 2000; 46 (28.22 per million bovines aged over 24 months) in 2001, 38 (25.75 per million bovines aged over 24 months) in 2002, 15 (10.54 per million bovines aged over 24 months) in 2003, 11 (7.882 per million bovines aged over 24 months) in 2004, 1 at 22 Apr 2005)
- France : 946 cases since 1991 (14.73 per million bovines aged over 24 months in 2000 (annual incidence rate in animals euthanised or found dead = 5.45; annual incidence rate in BSE clinical cases = 9.27;); 274 in 2001 (19.70 per million bovines aged over 24 months); 239 in 2002 (20.96 per million bovines aged over 24 months); 137 in 2003 (12.01 per million bovines aged over 24 months), 54 in 2004 (4.736 per million bovines aged over 24 months), 15 at 22 Apr 2005). > 301 200 cattle in France may have been infected with BSE since the disease first appeared in the 1980s to June 2000, based on the amount of meat and bone meal (MBM) from the United Kingdom used in France during the 1980s (46 000 tons between 1986 and 1990), and the fact that most cattle are infected with the disease between the ages of 6 to 12 months. There is uncertainty about estimates of the number of cases in the early 1980s, but the level of animals infected climbed between 1987 and 1990 and dropped from then until 1992. Furthermore, 47 300 animals at an advanced stage of the disease entered into the food chain before 1996, and 1500 between July 1996 and June 2000. According to previous official figures there were just 103 confirmed cases of the disease between 1991 and 2000, during which period the government relied on farmers and veterinarians to report animals with BSE. Since 2000, when controls were tightened, a further 820 cases have been confirmed, according to figures published last month, bringing the total to 923 over the past 13 years. The majority of beef cattle in France are slaughtered before 24 months of age. The infected animals would have been killed before the disease could have shown itself, because of BSE's long incubation period. In 1989, France banned the use of meat and bone meal in cattle feed. The law was modified only in June 1996 (almost 7 years after Britain) and 2000 to ban it from being fed to all ruminant feeds. Just 4 years ago, as France ignored a European Union ruling that British beef was safe again, infected cattle were still entering the food chain. The discovery of an apparent link between BSE and its human equivalent, vCJD, was made in 1996 and led to a worldwide ban on British beef. The ban was lifted by the EU 1999 but illegally maintained by France until 2002. Yet it was not until 2001 that France introduced compulsory tests for BSE in cows, older than 24 months, sent for slaughterref.
- Slovakia : 20 cases (5 in 2001 (18.34 per million bovines aged over 24 months), 6 in 2002 (18.73 per million bovines aged over 24 months); 2 in 2003 (6.74 per million bovines aged over 24 months); 7 in 2004 (24.635 per million bovines aged over 24 months); 0 at 22 Apr 2005)
- Czech Republic : 15 cases since 1987 (2 in 2001 (2.85 per million bovines aged over 24 months), 2 in 2002 (2.50 per million bovines aged over 24 months), 4 in 2003 (5.78 per million bovines aged over 24 months), 7 in 2004 (10.234 per million bovines aged over 24 months), 3 at 22 Apr 2005)
- Slovenia : 5 cases since 1987 (1 in 2001 (4.34 per million bovines aged over 24 months), 1 in 2002 (4.44 per million bovines aged over 24 months), 1 in 2003 (4.39 per million bovines aged over 24 months); 2 (including an animal born in Germany) in 2004 (4.585 per million bovines aged over 24 months); 0 at 22 Apr 2005)
- Germany : 362 cases since 2000 (1.07 per million bovines aged over 24 months in 2000; 125 in 2001 (19.97 per million bovines aged over 24 months); 106 in 2002 (17.02 per million bovines aged over 24 months); 54 in 2003 (8.71 per million bovines aged over 24 months), 64 in 2004, 15 at 22 Apr 2005; the number of BSE-positive cases detected in Germany since 2001, according to their respective years of birth, is as follows: 2 in 1992; 3 in 1993; 13 in 1994; 80 in 1995; 123 in 1996; 29 in 1997; 18 in 1998; 13 in 1999; 0 in 2000). The 1st case of BSE in native cattle is reported from Germany in 2000. However, according to EU's Geographical BSE-Risk (GBR) opinion, exported German cattle could have been contaminated since 1988
- Greece : 1 only case since 1987 in 2001 (3.3 per million bovines aged over 24 months)
- Liechtenstein : 2 cases between 1987 and 2000
- Luxembourg : 2 cases since 1987 (1 in 2002) (14.54 per million bovines aged over 24 months)
- Austria : 2 case since 1987 in December 2001 (in Lower Austria federal province) and in 2005. In the latter case an 11 year old cow from a small farm with 8 cattle and 2 pigs located in Riezlern, Bregenz district, Vorarlberg federal province, in the western part of the country, near the German border. The farm is not a member of a breeding association; there was never any purchase of animals. No live animals have ever been sold; all cattle to be slaughtered were taken directly to the slaughterhouse. The affected cow had ear tag number AT 138 752 583. It was born on 31 Mar 1994 at the farm and was found dead on 26 May 2005. The most recently born offspring of the affected cow (calf AT 583 539 672, born on 24 Jan 2005) was slaughtered on 26 Apr 2005. 2 offspring of the affected cow were still on the farm when the farm was quarantined (cow AT 777 654 242, born in 2002, and female calf AT 079 944 747, born in 2003, on pasture). Feed: concentrated feed, whole meal, beet. Since 2002, controls of feeding stuff providers are carried out every year in spring on the occasion of farm audits. The feeding ban was met completely. Before 1995, concentrated feed was imported from Germany. The affected cow was well-fed and delivered about 9 litres of milk per day. During the period prior to its death it showed movement disorders, with no improvement after hoof trimming. The head was held in a low position but there were no disturbances in excretion or behaviour. The owner ascribed the movement disorders to the age of the cow and did not consult a veterinarian. The Austrian Federal Ministry of Health and Women was informed of the suspicion of BSE by the German Federal Ministry of Consumer Protection, Food and Agriculture on 17 Jun 2005. The affected cow had been delivered to a rendering plant in Germany. Samples for BSE testing were taken in Germany. Due to the fact that the 1st rapid test was positive, the sample was sent to the German National Reference Laboratory in the isle of Riems on 16 Jun 2005. A rapid test made at Bavarian Department for Health and Food Safety (Bayerisches Landesamt fuer Gesundheit und Lebensmittelsicherheit, Dienststelle Oberschleissheim), Oberschleissheim, Germany, on 15 Jun 2005 was positive (twice). Immunohistochemistry made at Friedrich-Loeffler Institute, Riems, Germany, on 21 Jun 2005 resulted positive. All 7 animals were slaughtered and cremated. Agriculture Minister Josef Proell said it was a standard safety procedure in Austria for cattle older than 24 months that die of unknown causes to be tested for BSE. As this cow died unexpectedly in late May after showing suspicious signs including tiredness, it was tested. Feeding animal meal to farm animals has been banned in Austria since 1991. If one carefully reads the Opinion of EU's Scientific Steering Committee on the GBR (Geographic Risk of BSE) in Austria, adopted on 16 May 2002, the occurrence of a 2nd case, particularly in a cow born prior to 2001, should not be overly surprising. According to the opinion, Austria was exposed to a very high external challenge from 1980-2000 due to import of large numbers of live cattle (about 190,000) and large amounts of MBM (meat and bone meat; 45 000 tons according to the country or 95,000 tons according to Eurostat and other export statistics) from BSE-risk countries. While significant fractions of these imports most likely did not enter the Austrian BSE/cattle system it was very likely that the BSE agent was imported into the country. Taken account of the information available on the origin and use made of the imported cattle and MBM it was concluded that the external challenge from cattle imports was high for 1986 to 1995 and very high for the period 1996-2000. On the other hand, MBM imports were posing a very high external challenge throughout the period 1980 to 2000. Though feed controls have been implemented since 1990, cross-contamination still appeared until 2001, there are at present still 2 EU member-countries with only one recorded BSE case: Greece and Finland. Luxembourg, like Austria, has had 2 cases
- Denmark : 16 Danish-born BSE cases since 1987. 13 of the cases were diagnosed in Denmark (2000-1 (1.14 per million bovines aged over 24 months); 2001-6 (6.77 per million bovines aged over 24 months); 2002-3 (3.35 per million bovines aged over 24 months); 2003-2 (2.39 per million bovines aged over 24 months), 2004-1 (1.296 per million bovines aged over 24 months), 2005-Apr-22-0). 2 were diagnosed in Portugal and 1 was found in Italy. In 1992, there was one case in a cow imported from Scotland.
- Swedenref : a 12 year old domestic cow at a farm in Vastmanlandref in central Sweden showed signs of the illness on Mar 2, 2006 and tested positive on Mar 3ref. Sweden has not recorded any case, and is the only EU country of which the GBR rating is II, namely that "It is unlikely that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent, but it cannot be excluded". All other EU countries have been rated as GBR III, namely "BSE has been confirmed, or it is likely but not confirmed that one or several domestic cattle are (pre-clinically or clinically) infected with the BSE-agent". The 12-year-old beef cow of mixed Charolais breed was born on a farm of 50 cattle in Sweden. She was in late pregnancy, had shown difficulties in rising for approximately 2 weeks, did not respond to treatment, and was euthanized and sent to destruction to a rendering plant. Brain stem sampling was done in accordance with the EU legislation for BSE testing. The sample was positive in the rapid/screening test (Biorad TeSeE ELISA) with an OD value of 2,42 in the 1st testing, 2,76 and 2,88 in the 2nd testing of the same preparation and of 3,22 in the 3rd testing from a new brain homogenate (cut-off value for all the runs was 0,22). The confirmatory testing, conducted at SVA (National Veterinary Institute of Sweden), were Western immunoblotting (TeSeE Western Blot, Biorad) and immunohistochemistry employing F89/160.1.5 antibodies; both tests were positive. In the immunohistochemistry, 11 pieces of brain stem were analyzed; all of them showed diffuse granular positive immunostaining of the grey matter, including the BSE target brain areas. All TSE testing, including all the screening testing for Sweden, is conducted at SVA and is quality-certified. The current BSE-surveillance in Sweden involves testing of all fallen stock and all emergency slaughtered cattle above 24 months of age as well as a yearly random sample of 10,000 cattle above 30 months of age at normal slaughter. Between 2001 and 2005, > 170,000 cattle were tested; out of these, 46,700 were normal slaughter and 125,000 were fallen stock and emergency slaughter. All tested negativeref. An epidemiological investigation on the possible source of infection is currently underway. Sweden has followed the European Union's legislation on feed banning. Since January 2001, there is a total ban on the use of mammalian protein in feed to food animals in order to avoid any possible cross contamination of the cattle feed at the feed mills.
- Finland : 1 case since 1987 in 2001 (2.39 per million bovines aged over 24 months)
- Italy : 125 cases since 1987 (48 in 2001 (14.1 per million bovines aged over 24 months); 38 in 2002 (10.60 per million bovines aged over 24 months); 29 in 2003 (9.86 per million bovines aged over 24 months); 8 in 2004 (2.348 per million bovines aged over 24 months), 3 at 22 Apr 2005; 67 autoctonous - expecially Holstein Friesian and Brown dairy cattle -, 6 imported) with average age of 5.7 years have been detected by screening 960,000 animals.
- Croatia : a 5-year old cow tested positive on Feb 2006ref
- The Netherlands : 77 cases since 1987 (1.07 per million bovines aged over 24 months in 2000; 20 in 2001 (10.25 per million bovines aged over 24 months); 24 in 2002 (13.19 per million bovines aged over 24 months); 19 in 2003 (10.86 per million bovines aged over 24 months), 6 in 2004 (3.399 per million bovines aged over 24 months), 0 at 22 Apr 2005)
- Poland : 20 cases since 1987 (4 in 2002 (1.28 per million bovines aged over 24 months); 5 in 2003 (1.49 per million bovines aged over 24 months), 11 in 2004 (3.578 per million bovines aged over 24 months), 11 at 22 Apr 2005)
- North America :
- USA : since the 1st case of mad cow disease turned up in December 2003 in Washington state, about 375 000 animals have been tested for the disease, primarily those that appear sick. The nation's cattle herd numbers 96 million.
- 1 affected Holstein cow originated from a dairy farm in Alberta, Canada was found in a farm in Mabton, about 40 miles southeast of Yakima in the State of Washington. Several nations, including Japan, South Korea and Taiwan, halted U.S. beef imports just hours after the USDA announced it on December 23, 2003. Japan is the largest overseas market for U.S. beef, but the logic of why Japan is banning beef is obscure since they already have cases of BSE. The USA had imported about 125 million pounds and about 1000 cattle from countries that later discovered BSE during the period when BSE would have been incubating. Current plans call for testing up to 400 000 animals over a period of 12 to 18 months for BSE : that's 10 times as many inspections as the department planned to conduct prior to the discovery of the infected cow on 23 Dec 2003. Some lawmakers on Capitol Hill, however, have suggested that as many as 3 to 4 million of the 35 million cattle slaughtered every year must be tested to assess the health of the nation's herds.
- a 9 years old downer cow born before the August 1997 ban in Texas died in November 2004. Over 2004, the USDA has tested about 375 000 animals as part of an enhanced surveillance program and had found only 3 inconclusive results with ELISA. Those 3 were each further tested twice using the internationally recognized IHC method (2-3 days required to complete), and all came out negative. But the inspector general, an independent arm of the USDA, asked for an additional test because of some discrepancies in the initial findings. The office also asked USDA to use the Western blot method of testing (1-2 days to complete), which many scientists believe is more precise. The positive result was confirmed on Jun 10 2005 and that he held his 9 p.m.teleconference soon afterward. Another "experimental" test (probably an enhanced version of the "gold standard" test) was done that came up positive. It was unusual for a sample to test BSE-negative in one test and positive in another, but that it has happened in Europe. A sample of the animal's brain tissue was sent to the world reference laboratory for BSE in Weybridge, England, which using a combination of rapid, IHC and Western blot testing confirmed infection on 24 June : the animal's disease strain did not closely resemble the British-style strain found in the 1st mad cow, which was born in Canada and raised in Washington State. Instead, it was closer to a strain found in France -- a result, another scientist said, that suggested that the infection had come from a different pool of infected feed, possibly imported from France. At the same time these diagnostic tests were being run by Weybridge, USDA conducted its own additional tests. This is the 1st autocthonous US BSE diagnosis in some 388 000 samples tested. Japan, which used to buy more U.S. beef than any other nation ($1.4 billion annually), closed its market to American beef after the first mad cow case and has resisted strong pressure to reopen it. Japan, where more than 15 cows have tested positive for mad cow disease, now tests every cow slaughtered. Its government has asked U.S. producers to do the same, but the U.S. government has said the universal testing was not necessay. The Japanese government agreed in principle in October 2004 to resume beef imports from American cattle aged 20 months or younger, but insisted shipments would not resume until its independent commission declared U.S. beef was safe to eat. Current negotiations with South Korea center on beef from animals under 30 months. Scientists believe mad cow disease takes several years to incubate within an animal's nervous system, making young cattle far less risky. The USDA has also been trying to lift a U.S. ban on live Canadian cattle that was imposed after Canada's first BSE case in May 2003. The border was scheduled to reopen in March 2005, but a federal judge in Billings, Montana, ordered a temporary halt at the urging of beef ranchers and producers who argued the Canadian BSE-prevention system was inadequate. An appeal on that decision is scheduled for next month, and a full trial it scheduled for late in July 2005. Unfortunately the feed ban has not been uniformly enforced, so it will not be unexpected when the US has an animal affected with BSE born after the feed ban (BAB) was to have taken effect. Although feed manufacturers are complying with the rules, on-farm feed mixing appears to be under the radar screen of the Food and Drug Administration's (FDA) enforcement of the feeding ban. Although the feed ban rule was put into place by the FDA, it is the USDA that is charged with animal diseases and animal health. So when the feed ban is violated on a farm (for example, by on-farm feed mixing), FDA does not appear to have an enforcement arm; but as the disease has a long incubation, it is outside of the jurisdiction of the USDA. Again, it will not be surprising if the US has a BSE-affected animal that is born after the ban. Several errors occurred in the testing process in the USA: (1) The brain samples were frozen, which makes some tests harder. (2) Parts from 5 carcasses were temporarily mixed up. (3) No written records were kept. DNA tests showed that the cow was born and raised in a herd in Southeast Texas and was approximately 12 years old. It was sent to at 3D/4D Waco-based Champion Pet Foods plant in Texas and was selected for sampling on arrival. It sent a sample of the brain from the infected cow to a laboratory at Texas A&M University, where a test for BSE was inconclusive. The plant at which this animal was sampled is a 3D/4D pet food plant that does not handle animals for human consumption and, in this case, did not use the animal in the production of pet food. The animal remains were incinerated.
-
a
12-year-old animalwhich was destroyed after having trouble giving birth in April 2005. It was suspected of having mad cow disease but retesting by animal health laboratories in Britain and Iowa showed samples were negative - a 10 years old or older red crossbreed cow from Santa Gertrudis, Alabama (born prior to the feed ban being enacted in 1997) tested positive at western blot on 13 Mar 2006ref1, ref2, ref3
- Canada : 7 cases since 1987 (4 in 2006) :
- 4 cases in Alberta (the same province as the herd of origin of the single U.S. case) in 2003 (0.33 per million bovines aged over 24 months), Dec 2004 (0.149 per million bovines aged over 24 months) (7 years old), and Jan 2005 (Red Deer; a Charolais cow 81 months of age, born on 21 Mar 1998 on the same premisesref1, ref2). On Jul 10, 2006, a 50-month-old dairy cow from Alberta tested positive : the entire carcass has been incinerated and did not enter the human or animal feed systems. Given its age, the affected animal was exposed to BSE after the 1997 implementation of Canada's feed banref
- 1 in British Columbia (Mar 2006 : a 6-year-old dairy cow, developed BSE after the implementation of Canada's feed ban; no part of this animal entered the human food or animal feed systemsref1, ref2)
- 1 in Manitoba : a mature cross-bred beef cow purchased by the owner as part of an assembled group of cattle in 1992 tested positive on June 2006 : this means that the animal was at least 15 years of age and would have been born well before the 1997 introduction of Canada's feed ban. A calf born to the affected animal in 2004 is also being tracedref1, ref2.
- Israel : 1 case since 1987 in 2002 (6.25 per million bovines aged over 24 months)
- Japan : 14 cases (3 in 2001 (1.44 per million bovines aged over 24 months); 2 in 2002 (0.97 per million bovines aged over 24 months); 4 in 2003 (1.96 per million bovines aged over 24 months), 5 in 2004 (2.491 per million bovines aged over 24 months), 2 at 22 Apr 2005)
- Austria: 2,500; 100 (**)
- Belgium: 160 (*); 100 (**)
- Cyprus: 2500; 500
- Czech Republic: 40 (*); 100 (**)
- Germany: 650 (*); 500
- Denmark: 100 (*); 100 (**)
- Estonia: 210 (*); 100 (**)
- Greece: 10 000; 5000
- Spain: 62 750; 5000
- Finland: 30 (*); 100 (**)
- France: 46 500; 5000
- Hungary: 300 (*); 500
- Ireland: 450 (*); 100 (**)
- Italy: 30 000; 5000
- Luxembourg: 120 (*); 100 (**)
- Lithuania: 1360 (*); 100 (**)
- Latvia: 250 (*); 100 (**)
- Malta: 30 (*); 100 (**)
- Netherlands: 2400 (*); 500
- Poland: 8600 (*); 500
- Portugal: 6000 (*); 1500
- Sweden: 60 (*); 100 (**)
- Slovakia: 240 (*); 100 (**)
- Slovenia: 10 (*); 100 (**)
- UK: 780 (*); 500
- Spain - 36 (10.6)
- France - 16 (1.4)
- Germany - 21 (3.3)
- Belgium - 7 (4.7)
- Netherlands - 7 (4.0)
- Italy - 12 (3.6)
- Denmark - 2 (2.3)
- Ireland - 5 (1.4)
- Portugal - 13 (16.9)
- UK - 21 (4.2).
- atypical glycoform of PrPSc :
- an apparently healthy 23-month-old Holstein steer from Japanref
- bovine amyloidotic spongiform encephalopathy (BASE) : 2 healthy cows from Italy (one cow aged 11 years, Brown Swiss breed, from a mixed production (milk and meat) holding and one cow aged 15 years, Piemontese breed, from a beef cattle holding) found during compulsory screening. The disorder is pathologically characterized by :
- lacked evidence of vacuolar lesions
- presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases
- a different pattern of regional distribution and topology of brain PrPSc accumulation (the olfactory mucosa instead of the usual brainstem)
- Western blot analysis show a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc.
- France : 3 cases with higher molecular mass of the unglycosylated PrPres and PrPres strong labelling by P4 mAbref. Then other 6 affected cows aged from 8 years to 15 years with atypical glycoforms were found in departments of Loire-Atlantique (2 cases), Cotes-d'Armor (1 case), Creuse (1 case), Loire (1 case) and Jura (1 case). Genetic analysis of several of these atypical cases has ruled out the hypothesis of a polymorphism in the gene coding for the prion protein
- confirmations of "new" atypical BSE cases have recently been received from Belgiumref, Denmarkref, the Netherlands (similar to the French cases) and Polandref (similarities to Italian cases)ref, and USA (a 12-year-old Texas cow testing positive for BSE in June 2005, and the 10-year-old Alabama cow that tested positive in March 2006)ref1, ref2, ref3
- a manifestation of the BSE agent with different molecular features in cattle, as recently described following transmission in transgenic mice expressing the human prion protein. Mechanisms involved in such observations remain to be established, but it should be emphasized that such PrPres changes were only found following transmission of cattle BSE, not of human vCJD, to these human transgenic mice. Genetic differences in the prion genes between these atypical cattle and the general cattle population might be expected to give rise to variants in electrophoretic profiles of PrPres, as the sequence of the human PRNP gene is known to influence the molecular features of PrPres in some cases of human sporadic CJD. Sequencing of the entire ORF of the prion genes of 2 of the atypical cases that showed the known sequence for cattle excluded this hypothesis. Importantly, with regard to the single polymorphism described in the bovine prnp gene, which can contain 5 or 6 repeats of the octapeptide region, no differences were observed between the atypical and typical BSE cases, which could otherwise be distinguished by labelling with P4 mAb that recognizes an epitope very close to this region of the protein. In human sporadic CJD, it has also been shown that 2 distinct PrPres types could be inter-converted in vitro by altering their metal ion occupancy. Treatment with metal ion chelator EDTA, in the range of concentrations that was shown to modify the PrPres profiles in human CJD, did not modify the electrophoretic patterns of cattle-BSE cases. The differences between atypical cases and typical cattle BSE were maintained, with regard to both molecular mass of unglycosylated PrPres and P4 labelling of PrPres
- cattle may also have been infected by another source of infectious agent, such as scrapie from sheep and goats. Interestingly, experimental infection of cattle with a British natural sheep scrapie source indeed led to similar differences in the PrPres electrophoretic profiles compared to typical cattle BSE.
- a spontaneous rare sporadic form of these diseases could exist in cattle as in humans without an infectious origin, and might have been the origin of the BSE epidemic. As different PrPres profiles were found between sporadic and variant CJD in humans, this hypothesis might also explain our finding. Further studies are now required to determine the frequency of such novel molecular phenotypes in cattle and the biological features of the involved infecting strain. These may be carried out by means of mouse transmission studies in a panel of wild-type mice with different prnp genotypes, as well as in bovine transgenic mice
- the inadequacies of public information, particularly in the UK
- failure to prevent international spread through contaminated MBM
- 1. BSE Chapter of the OIE Terrestrial Animal Health Code
- 1.1 Red Muscle Meat : based on scientific information provided by world experts, the OIE Code Commission recommended the listing of deboned skeletal muscle meat among the list of safe commodities. The OIE incorporated deboned skeletal muscle meat into the list of commodities that can be safely traded regardless of the BSE status of countries. For this commodity to be traded freely, it has to meet certain conditions:
- it must exclude mechanically separated meat;
- it must come from cattle which were not subjected to an invasive stunning process, prior to slaughter (because this can drive brain material into the blood vessels in the muscle)
- cattle must have been subjected to an ante and post mortem inspection and cannot include suspect or positive BSE cases;
- the meat, during its processing, must be kept from possible contamination ith [BSE] specified risk material (SRM);
- it must come from animals 30 months old or younger.
- 1.2 Blood products : blood and blood products were also included in this safe commodity list. To be traded freely these products must come from animals which were not subjected to an invasive stunning process prior to slaughter [see 1.1 above].
- 1.3 Categorisation of countries according to the BSE risk : the 2004 OIE Terrestrial Animal Health Code recognized 5 different BSE risk categories:
- free
- provisionally free
- minimal risk
- moderate risk
- high risk
- a. negligible risk,
- b. controlled BSE risk,
- c. undetermined BSE risk.
- 2. Avian Influenza Chapter of the OIE Terrestrial Animal Health Code
- 2.1 Notification requirements and compartmentalization : the adopted chapter on Avian influenza incorporates several significant concepts that will lead to increased transparency in reporting and a more risk-based approach to trade recommendations. The new notification requirements include reporting on the presence of avian influenza, of low and high pathogenicity, in poultry. Poultry is defined to include all birds raised for commercial purposes, and the status of the country is determined only on the presence of AI in [domestic] poultry. This means that the presence of avian influenza in migratory water fowl should be notified without negatively affecting the health status of the country. Since Avian influenza is endemic in migratory water fowl, it is difficult to prevent poultry from becoming infected. The new Avian Influenza chapter incorporates the concept of compartmentalization, which describes the criteria for the separation of these 2 populations through biosecurity measures. Veterinary Services in conjunction with the industry can establish and enforce the necessary conditions to ensure the safety of a poultry subpopulation through compartmentalization, even when AI is found in the rest of the country.
- 2.2 Vaccination : the new chapter also incorporates criteria for trading commodities while vaccination is being applied as an additional tool for the control and eradication of AI. Vaccination should be carried out with approved vaccines and vaccination protocols identified in the OIE Terrestrial Manual.
- 3. Animal Welfare Chapters of the OIE Terrestrial Animal Health Code : standards on animal welfare, included in 4 chapters, were adopted (i.e. slaughter for human consumption, including religious slaughter; land and sea transport of animals; humane killing of animals for disease control purposes). For the 1st time, an organisation with a global mandate provides the international community with standards in this field.
- Mad Cow Disease background from USDA's Animal and Plant Health Inspection Service (APHIS)
- Q&A on BSE from APHIS
- Q&A from CDC
- Q&A on BSE for hunters from APHIS
- Background from APHIS
- Countries reporting BSE from 1989 to September 2003 from OIE
- Bovine spongiform encefalopathy (BSE), scrapie, Creutzfeld-Jakob disease (CJD) and the prion protein (PrP)
- The BSE Inquiry : the inquiry into BSE and vCJD in the UK
- BSE at Department of Environment, Food and Rural Affairs (DEFRA)
- Mad-cow.org (from April 16, 2001 "News" and "Policy" has moved to Organic Consumers Association)
- bovine viral diarrhea (BVD) virus may initially present very similarly to FMD but does not affect pigs
- malignant catarrhal fever (MCF) virus / Alcelaphine herpesvirus 1 (AHV-1)
- bovine papular stomatitis (BPS) virus causes a benign disease of cattle, endemic in the Western hemisphere.
- Demodex bovis : a species causing mange in cattle
- bovine leukemia, lymphomatosis or lymphosarcoma / enzootic bovine leukosis (EBL) / malignant lymphoma of cattle / bovine viral leukosis : a progressive fatal lymphosarcoma affecting adult cattle, caused by the bovine leukemia virus, and characterized by infiltration of lymphoid tissue throughout the body by malignant lymphocytes, with enlargement of lymph nodes and spleen. It occurs worldwide, in up to 5% of the cattle herd, and is more commonly found in dairy herds. Transmission is by close contact between infected and healthy animals or through the transfer of blood containing infected lymphocytes by instruments such as dehorning devices or hypodermic needles. Maternal transmission occurs in approximately 20% of calvings from infected dams. Mechanical transmission by biting flies is also possible.
- sporadic bovine leukosis : a disease similar to enzootic bovine leukosis, with malignant proliferation of lymphoid tissues but no culturable infectious agent; it occurs in three forms that vary in the age of the animal and organ affected: calf, seen in animals under 6 months of age and marked by generalized lymphadenopathy and widespread metastasis; thymic, seen in animals 6 to 18 months of age and confined mainly to the thymus; and cutaneous or skin, the only nonlethal form, affecting young adults and marked by cutaneous tumors that regress spontaneously
- contagious bovine pleuropneumonia or peripneumonia (CBPP) is a List A disease of cattle caused by Mycoplasma mycoides subsp. mycoides SC (bovine biotype) (SC: small colonies). It is manifested by anorexia, fever, and respiratory signs such as dyspnea, polypnea, cough, and nasal discharges. Diagnosis is direct. The main problems for control or eradication are the frequent occurrence of subacute or asymptomatic infections and the persistence of chronic carriers after the clinical phase. According to OIE's "Manual of standards, Diagnostic Tests and Vaccines 2000", Chapter 2.1.6., only one strain is recommended for preparing CBPP vaccines: strain T1/44, a naturally mild strain isolated in 1951 by Sheriff & Piercy in Tanzania. The 44th egg-passage is sufficiently attenuated to protect cattle without post-vaccination severe reactions. Post-vaccination reactions may occur at the inoculation site. Cattle breeds should be assessed for their sensitivity before mass vaccinationref. CBPP is endemic in Zambia. According to the 2004 annual report to the OIE, 47 outbreaks have been recorded and 450 000 bovines vaccinated
- brisket disease : a disease seen in young cattle at altitudes above 7600 feet, resembling altitude sickness of humans and often progressing to fatal respiratory or cardiac failure; it is sometimes seen in sheep and has been produced experimentally in pigs.
- Corridor disease : a highly pathogenic tick-borne protozoal disease caused by infection with Theileria parva lawrencei and transmitted primarily by the tick Rhipicephalus appendiculatus; lesions and symptoms are similar to those of East Coast fever but is less severe, and is highly pathogenic for cattle, with cape buffalo(Syncerus caffer) and cattle in eastern and southern Africa serving as a reservoir of infection.
- crooked calf disease : a syndrome of congenital skeletal defects seen in calves in the western United States and Canada when their mothers have eaten certain species of Lupinus during pregnancy; characteristics include joint contractures, torticollis, and spinal deformities.
- dermopathic herpesvirus disease : a herpesvirus disease of cattle, characterized by ulcerative lesions in the skin; it resembles lumpy skin disease
- circling disease : listeriosis in domestic animals.
- falling disease : a condition seen in cattle with dietary copper deficiency, sometimes with molybdenum poisoning; affected animals suddenly throw up their heads, utter a loud cry, and usually quickly die. They may show earlier signs of dietary deficiency such as diarrhea and depigmentation of the hair.
- farmer's lung disease of cattle : a disease in cattle similar to farmer's lung in humans, caused by hypersensitivity to moldy hay contaminated by Saccharopolyspora rectivirgula (a.k.a. Micropolyspora faeni) or Thermoactinomyces vulgaris.
- Tzaneen disease : a tick-borne protozoal disease, seen in South Africa, due to Theileria mutans, and occurring in cattle and water buffalo, which may manifest as a mild febrile disease or may be severe and fatal.
- sweating sickness / tick toxicosis : a febrile, tickborne illness affecting African cattle, especially calves, due to a toxin produced by Hyalomma truncatum, and characterized by the presence of moist eczematous lesions of the mucous membranes
- turning sickness : an unusual form of bovine theileriasis in which Theileria parva invades the central nervous system, causing either acute attacks of spinning followed by unconsciousness or chronic circling and incoordination
- teart disease of cattle : molybdenum poisoning in cattle that graze on teart, a type of English pasture in which the grass contains high levels of molybdenum.
- sweet clover disease : a hemorrhagic disease of animals, especially cattle, caused by ingestion of spoiled Melilotus (sweet clover), which contains the anticoagulant dicumarol.
- crazy cow syndrome : a type of neurotoxicity seen in cattle in the United States, Brazil, and South Africa after they have eaten any of various plants of the genus Solanum; characteristics include cerebellar damage with staggering and incoordination.
- fat cow syndrome / fatty liver disease / pregnancy toxemia in cows : a syndrome seen in overly fat cows just after they have given birth; loss of appetite postpartum leads to mobilization of body fat stores with deposition of fat in the liver and ketosis, sometimes ending in coma and death
- honker syndrome : a disease of feedlot cattle, of unknown etiology, characterized by edema of the lower trachea with dyspnea and a honking sound during inspiration.
- licking syndrome : a form of pica in cattle in which they lick their own or each other's hair and skin, or other surfaces; it is often due to dietary deficiency of copper or sodium.
- Akabane virus disease : the symptom complex seen in fetal sheep or calves after their mothers have been bitten by insects and infected with the Akabane virus; fetuses have encephalomyelitis or defective brains (sometimes hydranencephaly) and arthrogryposis
- isolation of a bovine enteric calici-like virus (a norovirus) associated with outbreaks of diarrhea which appears to be a recombinant with genes derived from 2 distinct viruses belonging to genogroup III has been reported in 2004ref
- lumpy skin disease (LSD) virusref1, ref2 : a List A highly infectious poxvirus disease
- bovine herpesvirus 1 (BHV1) / bovine rhinotracheitis virus (genus Varicellovirus)
- bovine herpesvirus 2 (genus Simplexvirus) => bovine ulcerative mammillitis.
- bovine parvovirus : a virus of the genus Parvovirus infecting cattle that causes diarrhea in calves; infection during the first or second trimesters of gestation may result in abortion. Infection is widespread and antibody to the virus can be found in a high proportion of adult cattle
- bovine enterovirus / ecbovirus : a species of viruses of the genus Enterovirus, separable into 2 serotypes, that have been associated with infertility and abortion in cattle
- Trichomonas foetus : found in the genital tract of cattle; it causes a contagious venereal disease (bovine trichomoniasis) transmitted from bulls to cows by coitus or by artificial insemination, and characterized by early abortion, pyometra, and sterility.
- Paramphistomum cervi (a.k.a. amphistom, Fasciola cervi) is relatively common in India, e.g., in Himachal Pradesh it can be found in some 15% of dairy cattle, 11% of buffalo, and 3-4% of small ruminants. Though normally a mild pathogen, it was blamed for bovine and ovine losses in Himachal Pradesh (Siroli and Hamirpur) in 1986.
- Ehrlichia ruminantium (a.k.a. Cowdria ruminantium)
- Onchocerca gibsoni : a species that produces subcutaneous nodular swellings on the legs of cattle and zebras.
- Haematopota : a genus of horse flies (family Tabanidae), large biting bloodsuckers that attack horses, cattle, and other mammals and cause anemia, mastitis, anthrax, anaplasmosis, and trypanosomiasis.
- derriengue : rabies, usually of the paralytic form, transmitted by vampire bats in Mexico, South and Central America, and Trinidad. It is usually seen in cattle, but infected bats may attack other domestic animals and even humans.
- derrengue [Sp. from derrengar to dislocate the hip] : a fatal neuropathy of cattle seen in El Salvador following ingestion of the plant Melochia pyramidata, characterized by weakness and paralysis starting in the hindlimbs and progressing forward. The South American name is mal de caderas
- epivag [epididymitis + vaginitis] : a venereal disease of cattle, probably of viral origin, in Kenya, southern Africa, and the United States, marked in cows by vaginal inflammation and discharge and by sterility. In bulls it is marked by epididymitis
- black leg / blackleg / symptomatic anthrax / blackquarter / quarter evil or ill : an acute anaerobic bacterial febrile disease of cattle and sheep caused by Clostridium chauvoei; symptoms include crepitant emphysematous swelling in the heavy musculature and a high fever, often leading to death within a day. Clostridium chauvoei occurs naturally in the intestinal tract of animals; contaminated pasture appears to be a source of organisms, which can remain viable in the soil for many years. The pastures in Masvingo seem to be heavily and somewhat permanently contaminated. Prevalent worldwide and not a zoonosis, blackleg is a not an OIE-listed disease. Most cases occur in cattle from 6 months to 2 years old; vaccination, if performed according to the prescribed regime, is safe and reliable (19990806.1356)
- imapunga : a rare disease of African cattle, closely related in pathology to African horse sickness
- vagus indigestion : a condition in cattle and sometimes sheep caused by damage to the vagus nerve, such as after traumatic reticuloperitonitis; characteristics include impaired motility through the stomachs and intestines, abdominal distention, chronic constipation, and anorexia
- lechiguana / bovine focal proliferative fibrogranulomatous panniculitis : a disease of cattle characterized by large, hard, subcutaneous swellings that grow rapidly and result in death after 3-11 months in untreated animals. Cattle treated with antibiotics recover. The disease has been reported from 5 states in south and southeastern Brazil. Histologically, the lesion consists of focal proliferation of fibrous tissue infiltrated by plasma cells, eosinophils, lymphocytes and sometimes neutrophils. The primary lesion is an eosinophilic lymphangitis, which results in eosinophilic abscesses, with occasional rosettes containing bacteria in their centres. Much experimental and epidemiological evidence, reviewed in this article, supports the suggestion that lechiguana is caused by an association of Pasteurella granulomatis (syn: Mannheimia granutomatis) and Dermatobia hominis (human botfly)
- fescue foot / fescue lameness or toxicosis / tall fescue lameness / fescue : a condition seen in cattle and sheep in Australia, New Zealand, and North America after they graze on tall fescue (Festuca arundinacea) contaminated by the fungus Acremonium coenophialum, which contains a toxic principle similar to that of ergot; characteristics include lameness of the hind feet that may progress to necrosis and dry gangrene and may spread to the ears and tail
- rumenitis : inflammation of the rumen.
- rumenotomy : surgical incision of the rumen of an animal to remove a foreign body or impacted food or to evacuate gases.
- omasitis : inflammation of the omasum
- abomasitis : inflammation of the abomasum.
- left displacement of the abomasum (LDA) : displacement of the abomasum of a cow to the left, underneath the rumen, with abomasal atony, usually soon after birth of a calf. It may be due to previous pressure from the gravid uterus or to abomasal distention from a high-grain diet. Symptoms include anorexia, drop in milk production, and ketosis.
- right displacement of the abomasum (RDA) : displacement of the abomasum of a cow to the right, with abomasal atony, usually soon after birth of a calf; it is sometimes due to obstruction of the pylorus. Symptoms include anorexia, drop in milk production, and a palpable fluid-filled organ on the right flank. It may progress to abomasal torsion, an emergency situation.
- abomasopexy : surgical fixation of the abomasum to correct right or left displacement of the abomasum
- abomasotomy : surgical cutting into the abomasum, usually to remove a bezoar or impaction
-
hemorrhagic septicaemia (HS) is an acute pasteurellosis, caused
by particular serotypes of Pasteurella
multocida,
a Gram-negative coccobacillus residing mostly as a commensal in the upper
respiratory tract of animals, and manifested by an acute and highly fatal
septicaemia principally in cattle and water buffalo; the latter are thought
to be more susceptible than cattle. It is a major disease of cattle and
water buffalo in Asia, Africa, and some countries of southern Europe and
the Middle East. The worst epidemics occur during the rainy season. HS
is most common in the river valleys and deltas of southeast Asia among
buffalo used in rice cultivation. The HS serotypes of P. multocida
have not been recovered from human infections. The principal means of prevention
is vaccinationref.
The disease has been recorded in wild mammals in several Asian and European
countries. In many Asian countries disease outbreaks mostly occur during
the climatic conditions typical of monsoon (high humidity and high temperatures).
The Asian serotype B:2 and the African serotype E:2 (Carter and Heddleston
system), corresponding to 6:B and 6:E (Namioka-Carter system), are mainly
responsible for the disease. In wild animals, serotype B:2,5 is predominantly
present. The association of other serotypes, namely A:1, A:3 with a HS-like
condition in cattle and buffaloes in India has been recorded. HS has been
erroneously and widely used as a synonym for shipping fever and other infections.
The result has been that the disease has been mistakenly reported in South
America and elsewhere. There was similar confusion in the 1940s, and the
differences between the diseases have been clarified. HS and shipping fever
are separate conditions caused by different bacteria (Pasteurella multocida
vs Mannheimia haemolytica). Unlike HS, shipping fever is not septicaemic
nor does it cause multisystemic petechial haemorrhages. The clinical manifestations
of the typical disease caused by B:2 or E:2 strains include a rise in temperature,
respiratory distress with nasal discharge, and frothing from the mouth,
and leads to recumbency and death. Infection with serotypes A:1 and A:3
predominantly involves pneumonia resulting in mortality. Septicaemia is
the characteristic feature in all the disease conditions. The incubation
period varies from 3 to 5 days. In peracute cases, there may be sudden
death with observable clinical signs. Buffaloes are generally more susceptible
to HS than cattle and show more severe forms of disease with profound clinical
signs. Subcutaneous oedema from the mandible to the brisket is one distinctive
feature of the disease in endemic areas; most deaths are confined to older
calves and young adults. Massive epizootics may occur in endemic as well
as non-endemic areas. In the recent past, HS has been identified as a secondary
complication in cattle and buffalos following outbreaks of foot and mouth
disease (FMD). Case fatality approaches 100% if treatment is not followed
at the initial stage of infection. The diagnosis of the disease is based
on the clinical signs, gross pathological lesions, morbidity and mortality
patterns, and confirmation by isolation of the pathogens and their conventional
and molecular characterisation. For references, as well as for Detailed
Diagnostic Techniques and Requirements for Vaccines and Diagnostic Biologicals,
refer to chapter 2.3.12 of the Manualref.
The disease is endemic in Thailand, affecting mainly buffaloes; preventive
vaccination is practiced
- ruminal tympany / bloat : a kind of indigestion in cattle and sheep, marked by an abnormal collection of gas in the rumen; the usual cause is a diet too high in carbohydrates. As gas volume increases, the rumen presses against adjacent organs; it may occlude the vena cava and cause circulatory problems or press against the diaphragm and lungs and cause death from asphyxia
- primary ruminal tympany / frothy bloat : ruminal tympany caused by eating too much wet or frothy legume, particularly alfalfa or clover, which forms a stable foam in the rumen
- secondary ruminal tympany / gas bloat : ruminal tympany caused by an esophageal obstruction that prevents eructation
- bovine ergotism is caused by a fungus known as Claviceps purpura or Claviceps paspalum. Essentially, ergot can be divided into 2 categories, the neurological form that causes animals to stagger (C. paspalum) and the gangrene form (C. purpura). This form causes vasoconstriction such that cattle may slough their ears, the switch of their tail, or, even their hooves. It is very painful when they slough their hooves. The animals will not walk to feed or water, and euthanasia is the best option. If the animal has the neurological form of the disease, they can recover, but there is no treatment for the gangrene. The fungus invades the seed head and forms a sclerotia, which is approximately twice the size of the individual grains in the seed head. It is visible, and, if producers are aware that the conditions for the fungus are right, they may be able to examine their hay fields and avoid baling infected grasses
-
Clostridium botulinum
(bovine botulism) : cattle demonstrate a lack of tone in the muscles,
progressively become weak and ataxic. The weakness is because the toxin
interrupts the nerve impulses to the muscles, producing a flaccid paralysis.
Many cows will lie down in what is described as a "milk fever" position,
that is turning the head to flank. The flaccid paralysis produces abnormal
facial expressions with droopy eyelids, drooling and lack of ability to
grasp food with the mouth. The tongue may hang out of the mouth due to
lack of muscle tone (often considered a classical sign of botulism in cattle).
The rumen activity ceases, bloat and hard, dry manure are present. The
clinical signs vary widely because of the wide range of times between exposure
and onset. Generalized weakness may persist for weeks. There are no clinical
or distinctive pathological signs of disease to indicate the signs are
specifically due to botulism. The toxin may be detected in the blood, the
rumen contents or the feed. It is the toxin that is detected, not the bacteria
responsible for production of the toxin. Mouse bioassay, injecting the
suspect toxin into the mouse and waiting for death or clinical signs in
the mouse, is often done. Samples are injected into mice, some of whom
have been protected by specific botulism antitoxin. Culture of the bacteria
is difficult, it is an anaerobic bacteria, and conditions must be right
for the bacteria to produce the toxin. Vaccines against Cl. botulinum
toxins types C and D in cattle and other farm animals (small ruminants,
horses) are available and widely applied in countries such as Australia,
South Africa, and Israel.
- lamziekte [Afrikaans “lame-sickness”] : a type of botulism seen in cattle in South Africa after they chew on infected or putrefying bones in an effort to compensate for a phosphorus deficiency.
- bovine babesiosis / redwater fever / Texas cattle fever : infection of cattle by Babesia; the acute phase is manifested by fever, hemoglobinuria, anemia, icterus, and splenomegaly
- Babesia argentina : an etiologic agent of bovine babesiosis in Central and South America, transmitted by Boophilus microplus, and in Australia, transmitted by B. microplus and B. australis.
- Babesia bigemina : an etiologic agent of bovine babesiosis in Central and South America, certain regions in Europe, North, Central, and South Africa, the Middle East, the West Indies, and formerly the southern United States, which is transmitted by various ticks, especially Boophilus annulatus and B. microplus. It has been largely eliminated by eradicating its tick vector
- Babesia divergens : an etiologic agent of bovine babesiosis in temperate regions of northern, western, and central Europe and perhaps Asia, transmitted chiefly by the ticks Ixodes ricinus and Haemaphysalis punctata.
- Babesia major : an etiologic agent of bovine babesiosis, transmitted by the tick Boophilus calcaratus, and occurring in North Africa, Europe, and the former Soviet Union.
-
cattle polioencephalomyelitis (leukoencephalopathy) : before Christmas
2003 a milking heifer in Cumbria in England, just south of the Scottish
border, was affected by paralysis for 5 to 6 days, followed by death. The
present case became recumbent following progressive flaccid paralysis over
5 to 6 days. Flaccid paralysis is normally thought to be a sign of lower
motor neuron (LMN), peripheral nerve, or neuromuscular junction (NMJ) disease.
This would suggest a lesion in the spinal cord, peripheral nerve, or muscle
rather than a lesion higher up in the CNS. Moderate weakness, hind-limb
ataxia and a slightly stiff gait were also noted in a 2nd heifer, which
gradually recovered over several weeks. The recumbent heifer was euthanised
and submitted to the Veterinary Laboratories Agency (VLA) - Penrith for
a PM examination. No macroscopic lesions were noted. Histological examination
revealed subacute bilateral non-suppurative and necrotising polioencephalomyelitis,
characterised by perivascular cuffing, glial nodule formation and occasional
neuronal necrosis, mainly involved dorsal and ventral horns (first cervical
segment of the spinal cord), medullary reticular formation, vestibular
complex and red nucleus, lesions suggestive of a viral infection in the
brain. Immuno-staining for Louping
ill virus (LIV)
(the only cause of encephalitis of this distribution and character currently
recognised in ruminants in the UK), bovine
herpesvirus type 1 and West
Nile virus (WNV)
antigens were negative. Joest-Degen
bodies
and Negri bodies
characteristic of Borna disease virus and lyssavirus infections (respectively)
were not detected. There was no evidence of a Transmissible Spongiform
Encephalopathy. Amazingly, NO EM work is reported, which could clarify
rabies or the fascinating clues to morbilli/paramyxovirus involvement.
Rabies was not given as a differential diagnosis in the UK case, and apparently
not excluded -- the absence of typical lesions and of Negri
bodies
mentioned is not conclusive. There are numerous reports of lyssaviruses
(rabies group viruses) in bats in Europe, including the UK, on an infected
bat that bit a woman. Why were there no viral isolation attempts in mice
or tissue culture, or brain histo-chemistry for lyssaviruses? 10 in-contact
heifers, including the recovered animal, were seronegative for louping
ill. The differential diagnosis of tetraparesis/paralysis in cattle includes
botulism, metabolic disturbances including hypocalcaemia, trauma, breed-related
disorders and viral encephalitides such as louping ill. Here we report
a case of in a Holstein heifer with a provisional clinical diagnosis of
botulism, based predominantly on the clinical findings of flaccid paralysis.
Further reasons for the suspicion of botulism were the presence of a dead
crow in the water trough in the field; that there was a large chicken broiler
unit 3 km from the farm; and that there had been a previous case of suspected
botulism, 3 months previously, at a neighbouring farm 1 km away. Although
no definite source was identified in that case, the clinical signs and
history were typical, and no alternative diagnosis was obtained in PM examination.
The differential diagnoses of bilateral polioencephalomyelitis in man are
neurotropic viral infections and paraneoplastic encephalosis (Love and
Wiley 2002). Over the last 10 years, 21 similar cases (ovine and bovine
non-suppurative and necrotising polioencephalomyelitis characteristic of
neurotropic viral infection but negative for louping ill antibody and/or
antigen) from 13 premises throughout England have been identified by the
VLA as a result of their examination of routine submissions. The VLA carries
out extensive surveillance and diagnostic work on material submitted by
private vets for their farming clients. In the submission of the material,
a diagnosis is not reached in every case. A full set of laboratory data
is not available from many cases, because these were identified retrospectively.
However, preliminary laboratory data, immunohistochemical results and lesion
distribution strongly suggest that the lesions observed in these sheep
and cattle are unusual or new presentations of encephalitis caused by a
known virus or one or more novel viruses. It is possible that the causative
agent is a common ruminant virus that is only occasionally neurotropic,
for example, an enterovirus. In similar cases of viral-type encephalitis,
a series of 51 cattle in Switzerland diagnosed over a period of 10 years
were examined retrospectively to investigate whether they constituted one
or more distinct diseases, and to search for etiological agents. PCR amplification
for chlamydial DNA was negative in all but 1 of 32 specimens. Immunohistochemistry
did not demonstrate the presence of chlamydial antigens, either in the
one PCR-positive case or in the other cases examined. Immunohistochemistry
for rabies virus, Borna disease virus, and central European tickborne encephalitis
virus was negative. In 4 cases, immunolabelled cells were found in the
lesions with antibodies against paramyxovirus antigensref.
In the absence of a reliable confirmatory test for botulism in cattle,
this case illustrates the importance of ruling out other possible causes
of tetraparesis/paralysis in cases of suspect botulism. Though this might
just reflect the highly efficient Swiss veterinary surveillance system
without -- in the current case -- BSE-related implications, interestingly
Switzerland was the 1st country in continental Europe to identify, as early
as 1990, endemic BSE. There is anedocotal evidence for an outbreak in cattle
of polio-like disease in the USA 30 or 40 years ago. The recent case is
also reminiscent of similar cases reported in the 1970s in the USA and
in Germany. In 1995 a paperref
by a German group described the isolation of a viral agent from brain explants
of a 15 month old heifer with clinical signs of sporadic encephalomyelitis.
The nucleocapsid structures were reminiscent of those of paramyxoviruses,
and positive fluorescence reactions were obtained with sera obtained from
sub-acute sclerosing panencephalitis (SSPE) patients and with rabbit hyperimmune
anti-rinderpest virus antiserum. In 1979 a similar paper was published
detailing a case from the USAref.
The virus was found in an animal experimentally infected with malignant
catarrhal fever virus. Again in indirect fluorescence tests, the agent
reacted with both measles and rinderpest virus antisera, and the authors
stated that this was the 1st report of a morbillivirus isolation from North
American cattle. In 1994, during the course of a project to complete the
sequence of the rinderpest virus genomeref,
we found very major differences in the sequence of the matrix (M) protein
gene derived from our virus isolate from that which had been published
by an American groupref.
The difference in isolates was that Limo & Yilma had sequenced the
purported wild type virus and we had sequenced the vaccine strain derived
from this virus. Curiously all the other genes of the 2 viruses showed
>97 per cent identity. We independently sequenced the wild type strain
derived from a different source and found it to be almost identical to
our vaccine strain sequence. The conclusion we came to was that the American
sequence was derived from a contaminating virus present in the primary
bovine cells used to culture the virus for sequencing, which was most likely
related to the unknown morbillivirus-like viruses found in the previous
bovine cases. In addition, it was noted that one of the unvaccinated control
animals used in a vaccine trial to test vaccinia recombinant viruses at
the Plum Island laboratory in New Yorkref,
had cross-neutralizing antibodies to rinderpest virus prior to challenge,
indicating exposure to another morbillivirus. The animal was not protected
from rinderpest, however. A similar virus could be the causative agent
of the current meningoencephalitis case. If the aetiological diagnosis
of enterovirus infection were substantiated for the other cases, the species
specificity of such viruses would, almost certainly, rule out any pathogenicity
for man based on currently available evidence. In addition, as enteroviruses
are easily destroyed by heat, pasteurisation and cooking provide additional
safeguards if milk or meat from affected animals were to have entered the
food chain.
-
each year, the dairy industry loses billions of dollars to mastitis,
an infection of cows' milk glands. Now researchers have succeeded in genetically
engineering cows to resist this disease. The bacterial infection causes
inflammation and swelling, and a loss in milk production. Combined with
the cost of treating the disease, this adds up to a loss of about $2 billion
a year in the United States, and $200 million in Britain. Technological
advances that make it possible to collect more milk also make mastitis
harder to contain. We've increased their yield with the milking machine,
which spreads infections from cow to cow. One bacterium that commonly causes
mastitis,
Staphylococcus aureus,
is notoriously resistant to treatment: only 15% of infections are cleared
up by antibiotics. The medications often fail to fully penetrate the mammary
glands, leaving the surviving bacteria to wreak havoc yet again. To solve
this problem, a team of US researchers turned to genetic engineering.5
adult Jersey transgenic cows were created carrying the gene for the S.
simulans protein lysostaphin.
This allows them to produce a protein, normally created by S. simulans,
that kills S. aureus. The 3 that underwent testing showed significantly
better resistance to S. aureus infection than their non-transgenic
counterparts. This is the first time that biologists have created transgenic
cows that resist disease. Previous attempts to improve animals' disease-fighting
abilities have used chickens and sheep. Using genetic engineering to tackle
mastitis represents a judicious use of the technology. This technology
is very powerful, but so is selective breeding : so we did not want to
'waste' genetic engineering on a task that animal breeders could already
achieve. That made mastitis an attractive target, because breeding for
mastitis resistant cows has not been very successful. Of the mammary
glands infused with the mastitis bacteria cultures, only 14% became
infected in the 3 transgenic cows compared with 71% in the control animals.
The transgenic cow that produced the greatest amount of lysostaphin never
became infected. Does the lysostaphin protein present any problems if ingested
by humans? The researchers do not believe so. It seems not to attack any
protein produced by mammals, and therefore is unlikely to be harmful to
the cow or the consumer. However, Biggs is sceptical that farmers will
buy cows altered by genetic engineering. Products such as beef have a chequered
history because of mad cow disease, but milk has a squeaky clean image.
Genetic engineering may decrease mastitis incidence, but if consumers vote
with their feet then those cows aren't going to have a future. This advance
does not cure all types of mastitis. This is only targeted at one of the
pathogens causing mastitis, so the benefits would be concentrated in only
those herds that have problems with S. aureus. It's a contagious
germ that can be controlled with good hygiene and good milking practices.
This is a neat technology, but it's not a substitute for all of the other
prevention practices. Wall does not expect these transgenic cows to appear
in the dairy industry in the immediate futureref
- California mastitis test (C.M.T.) (for subclinical mastitis in cows): equal amounts of milk, bromcresol purple, and an anionic surface-active substance are mixed in four separate cups within a plastic paddle by rapidly rotating the paddle horizontally; a positive reaction is indicated by various degrees of gel formation, according to the degree of abnormality of the milk.
- Hotis test (for mastitis in cows): fresh milk containing bromcresol purple is incubated for 24 hours; a positive reaction is the formation of yellow flakes on the sides of the test tube
- Tragelaphus
- Tragelaphus angasii (nyala)
- Tragelaphus oryx (a.k.a. Taurotragus oryx; eland)
-
Tragelaphus
strepsiceros (greater kudu) : Bacillus
anthracis.
A unique outbreak of rabies virus
in kudu antelope began in central Namibia in 1977, apparently involving
oral spread of infection between individuals. It peaked in 1980 and eventually
subsided in 1985, by which time it caused an estimated loss of 30-50 000
antelope, or 20% of the population. During 2002 there was another substantial
outbreak in kudu, during which an estimated 2500 animals on > 81 farms
in Namibia died. This outbreak continued into 2003. The social behaviour
of kudu was believed to be related to the spread of rabies, and it is thought
that mouth lesions from the browsing of thorn-bushes may have been a contributing
factor due to the presence of the rabies virus in saliva. The kudu epizootics
in Namibia have provided an example of non-bite transmission, with horizontal
spread between kudus. Recent molecular studies in a panel of 37 rabies
virus isolates originating in Namibia between 1980 and 2003 suggested that
these viruses were all of the canid rabies biotype of southern Africa.
The viruses from kudu were closely associated with jackal, bat-eared fox
and domestic dog isolatesref
- Caprinae
- Capra
-
Capra
hircus (goat) : Taenia
multiceps,
Dicrocoelium
dendriticum,Trichostrongylus
colubriformis,
Trichostrongylus
probolorus,
Trichostrongylus
vitrinus,
Dermatophilus
congolensis,
Bacillus
anthracis,
Burkholderia
pseudomallei,
Yersinia
pestis,
Coxiella
burnetii,
orf
virus / contagious pustular dermatitis virus / ecthyma contagiosum virus,
Nipah
virus
-
stools : Enterocytozoon
bienuesi
-
milk : Russian
Spring-Summer encephalitis virus,
Tick-borne
encephalitis virus (TBEV) / Central European encephalitis virus,
Mycobacterium
avium subsp. paratuberculosis
(Johne's disease / chronic dysentery of cattle
/ paratuberculosis)
-
nerve tissue : PrPSc
- the prevalence of (clinical) cases of scrapie is believed to be much lower in goats than in sheep. Since April 2002, the EU member countries have intensified their surveillance activities in small ruminants, adding healthy animals at slaughterhouses to the previously tested risk- and clinically-suspect animals. During 2003, 37 561 healthy goats were tested in the EU member-states, of which 16 -- in 5 countries -- were found TSE-positive. The following table presents the published figures from the said countries:
- Country / appx adult goat population / healthy goats tested / TSE-positive
- Greece / 3 900 000 / 6425 / 9
- Spain / 2 330 000 / 6553 / 1
- France /1 030 000 / 11 223 / 3
- Italy / 820 000 / 3571 / 2
- UK / 88 000/ 193 / 1
- sheep -- 173 572 animals tested, 833 positive, 428 pending
- goats -- 17 294 tested, 47 positive, 52 pending.
- on 28 Oct 2004, the European Commission announced a possible finding of BSE in a 2.5-yrs old goat of a herd which totaled 600 animals, including 300 adults, slaughtered in 2002 in France. The entire herd had been culled and all the adult goats were tested for scrapie at that time, with negative results. All the carcasses, including that of the affected goat, were destroyed. In accordance with EU procedures, the finding was submitted to the Community Reference Laboratory (CRL) in Weybridge for evaluation by an expert panel and views are expected at the end of January 2005ref. Although BSE had never before been found naturally occurring in goats, the possibility that it could exist, masked by scrapie, has been acknowledged for some time. This is because it is likely that some goats ate the same feed that spread BSE in cattle, and laboratory experiments have shown that BSE can be transmitted to sheep and goats. As a result, precautionary measures, such as SRM controls, have been in place for some time to minimise any potential risk to public health. In its opinion of April 2002, the EC Scientific Steering Committee (SSC) recommended additional measures to protect public health in the event that BSE should become likely in small ruminants. In view of the possible finding of BSE in a French goat, the Commission is proposing that the additional measures recommended in the SSC opinion should be implemented, if the finding of BSE is confirmed. The draft EC proposal was discussed at an EU TSE Working Group meeting on 30 Nov 2004 and will be subject to further discussions at SCoFCAH (Standing Committee of Food Chain and Animal Health) in December and January. As the proposal currently stands, the list of tissues designated specified risk material (SRM) in goats will be extended to include:
- the whole alimentary canal;
- the organs, including lymph nodes, of the thoracic and abdominal cavities;
- the pre-femoral and pre-scapular lymph nodes;
- the entire head;
- the tonsils.
- France : 26 cases
- Greece: 12 positive, 0 pending (all positives were TSE suspects). Spain: 0 positive, 2 pending (in "risk animals").
- Portugal: 0 positive, 48 pending (3 in "risk animals," 45 in "healthy animals").
- Cyprus: 8 positive, 0 pending. (All the positives in "risk animals").
- Demodex capri : a species causing mange in goats
- caprine arthritis-encephalitis virus (a lentivirus, 1st identified in 1974) => caprine arthritis and encephalitis (CAE) is a lifelong infection and manifests as arthritis in adults and encephalitis in kids (not children but juvenile goats) 2-6 months old. Other clinical presentations can include a hard udder or mastitis, hypogalactia, chronic interstitial pneumonia, and progressive weight loss. CAE is a herd problem best prevented by maintaining a closed herd. Culling of positive animals and other segregation strategies can help to prevent horizontal transmission. Australia and New Zealand have voluntary CAE accreditation programs. The first outbreak in Bosnia & Herzegovina occurred in April 2005
- Ovibos
-
Ovibos
moschatus moschatus (muskox) : orf
virus / contagious pustular dermatitis virus / ecthyma contagiosum virus
- Ovis
-
Ovis
aries (sheep) : Taenia
solium,
Taenia
multiceps,
Dicrocoelium
dendriticum,
Trichostrongylus
colubriformis,
Trichostrongylus
orientalis,
Trichostrongylus
probolorus,
Trichostrongylus
vitrinus,
Trichinella
spiralis,
Dermatophilus
congolensis,
Toxoplasma
gondii
(the feral cat is a well-known reservoir in Tasmania. Previous studies
have found approximately 50% of cats infected. So called "abortion storms"
have been described from other parts of the world, referring to epidemics
of abortions in pregnant sheep when they are let loose on fields heavily
contaminated with oocysts. Preventing feral cats from shedding oocysts
on grazing land is difficult, and the best strategy is immunization of
pregnant sheep), Bacillus
anthracis
(livestock anthrax is now widespread throughout Indonesia and an endemic
problem in West Java), Brucella
melitensis biovar Ovis
(according to Bulgaria's declaration, the animal population in this country
has been free of B. melitensis (in sheep and goats) since 1941 and
of bovine brucellosis, B. abortus, (in cattle) since 1958. In contrast,
Greece is moderately (or even more) infected with B. melitensis
(68 outbreaks in 2003) as well as with B. abortus (221 outbreaks
in 2003). B. melitensis is the species that is generally regarded
as more pathogenic to humans),
Burkholderia
pseudomallei,
Yersinia
pestis,
Coxiella
burnetii,
Mycobacterium
avium subsp. paratuberculosis
(ovine Johne's disease (OJD) / chronic dysentery
of cattle / paratuberculosis), orf
virus / contagious pustular dermatitis virus / ecthyma contagiosum virus,
Rift
Valley fever virus
(more susceptible than cattle), Louping
ill virus (LIV)
(so far, this tick-borne viral encephalitis, which affects mainly sheep,
has been restricted to the British isles; a closely related disease of
sheep has been reported from Norway, Bulgaria, Turkey, and the Basque region
in Spain),
Wesselsbron
virus (WSL),
foot-and-mouth
disease virus (FMDV);
sarcoptic
mange (scabies): in sheep, this condition, caused by Sarcoptes scabiei
var ovis, is rare (reportable in the USA). It affects the non wooly
skin, usually starting on the head and face. In goats, S scabiei
var caprae is responsible for a generalized skin condition characterized
by marked hyperkeratosis. Lesions start usually on the head and neck. The
causative mite should be differentiated from Psoroptes ovis infestation,
a reportable disease in many countries (including the USA), characterized
by large, scaly, crusted lesions which develop almost exclusively on wooly
parts of the body. Intense pruritus manifests by biting and scratching.
Left untreated, sheep often become emaciated and anemic. In cattle, Sarcoptic
mange is a very contagious disease, spread by direct contact or indirectly
by fomites. The causative mite, Sarcoptes scabiei var bovis,
can be transmitted to humans and is a reportable disease. Lesions start
on the head, neck, and shoulders and can spread to other parts of the body;
pruritus is intense. Papules develop into crusts, and the skin thickens
and forms large folds. The whole body may be involved in 6 weeks. Diagnosis
is made by deep skin scrapings, skin biopsy, or response to therapy. All
the said mites should respond to ivermectin
-
stools : Echinococcus
granulosus
- Taenia ovis
- Demodex ovis : a species causing mange in sheep.
- hoose / husk : verminous bronchitis in sheep, cattle, goats, and swine, caused by the presence of nematodes of genera Dictyocaulus, Metastrongylus, Muellerius, and Protostrongylus in the bronchial tubes or lungs; it is marked by cough, dyspnea, anorexia, and constipation
- maedi-visna virus (MVV) => maedi-visna / ovine progressive pneumonia : a chronic viral disease of sheep, characterized by progressive weight loss and dyspnea that can be fatal. A demyelinating meningoencephalitis may occur, with paresis of the hind limbs progressing to total paralysis and death. The virus was originally isolated in the Iceland and causes a respiratory form characterized by pneumonitis (maedi [Icelandic “dyspnea”]), or a meningoencephalitic form characterized by paralysis and wasting (visna [Icelandic “wasting”]) in sheep (Brit.Vet.J. 100, 255-270). In Portugal, the number of infected animals was 34.4% in 1995, while the prevalence of the infection in flocks reached almost 82% (Rev.Portuguesa Ciencias Vet., XC(514), 66-70). The genome of MVV has 3 major genes, gag, pol, and env, which encode the virus structural proteins. The core proteins p16, p25, and p14 are encoded by the gag gene, while pol encodes the virus polymerase, and env encodes the envelope glycoproteins gp41(TM) and gp135(SU)ref.
- bluetongue (BT) disease virus (BDV). There are 24 serotypes worldwide. It is a noncontagious viral disease of sheep, wild ruminants (deer, elk, and pronghorn antelope), and rarely cattle (usually considered subclinical sentinels), goats, and carnivores. Infection is much more common than disease. Bluetongue infection and disease have been reported on all continents (northern Australia) except Antarctica. The viruses are biologically transmitted between ruminants by the biting midge Culicoides variipennis and Culicoidessonorensis in the USA. Other biting insects are likely the mode of transmission in other countries (in Spain notably Culicoides imicola, and according to some recent investigations, potentially also other species such as Culicoides obsoletus and Culicoides pulicaris), while bovines serve as the reservoir or rather amplifier of the virusref1, ref2. Infected cattle usually don't become noticeably ill because they carry the virus for a few months after infection. Signs most frequently seen include swollen cyanotic (blue) tongue, lameness, and muscle necrosis. Fatality rates are normally > 30% and animals which recover tend to remain unhealthy. Clinical signs are presumptive, and confirmation is based on identification of virus by isolation in embryonated chicken eggs, susceptible sheep, or cell cultures, or by PCR. Vaccines are available in other countries as well, but the practice of preventive bluetongue vaccination is most widely used in southern Africa. Use of serotypes other than the one(s) causing infection afford little or no protection. Killing affected or exposed sheep for the control of bluetongue is unlikely to be an effective, or scientifically justifiable policy. Viraemic cattle generally do not show clinical symptoms, while the duration of their viraemia is generally longer than in sheep. The value of quarantine and movement restrictions in sheep is also questionable. It has been postulated that a seasonal, annual introduction of BT-infected culicoides prevails in the Eastern Mediterranean, the vectors carried by the Persian trough (counter-clockwise) airstream during the second half of each year. This introduction usually affects Syria, Lebanon, Israel, Jordan, and (mainly southern) Turkey, while Cyprus is affected only sporadically -- once every several yearsref. The last Iberian outbreak in 1959 resulted in approximately 200 000 sheep deaths. Such a wind-borne introduction of BT virus occurred in 1977 and March 2004 in southeast Famagusta district. 5 BTV serotypes have been identified since 1998 in southern Europe: BTV 1, 2, 4, 9, and 16. The 1st incursion of BTV 16 to (southeastern) Europe was reported from Greece in 1999ref. No seroconversions (of any BTV serotype) in sentinel bovines were recorded in Greece during 2002 or probably also during 2003ref. Morocco is infected with BT 10, while neighboring Algeria and Tunisia are infected with BT 2. Many of the major islands in the Mediterranean are infected with various BT strains. The countries involved in 1997-2004 Mediterranean epidemic areref :
- 1997 : Greek islands
- 1998 : Greek islands
- 1999 : BTV-2 was reported from mainland Greece, Turkey, Bulgaria, Algeria, Tunisia, then spread along the western Mediterranean basin to Algeria, Corsica Island (France), Sardinia Island (Italy), and Menorca and Mallorca Islands (Spain, collectively known as the Balearic Islands). Since then, the virus seems to have been established in the said territories, demonstrating the typical seasonality which reflects the seasonal activity of the relevant culicoides vectors.
- 2000 : Italy (except northern regions), Turkey, Bulgaria, Algeria, Tunisia, France (Corsica), Spain (Balearic islands)
- 2001 : Italy (except northern regions), mainland Greece, Macedonia, Bulgaria, Kosovo, France (Corsica), Croatia, Serbia
- 2002 : Albania, Bosnia & Herzegovina, Bulgaria, Serbia
- 2003 : Italy (except northern regions; Calabria and Sicily; BTV 4 in Sardinia on 19 Sep; antibodies against BTV 16 were reportedly identified for the 1st time in Italy on 31 Jul in Puglia in sentinel animals), France (BTV 4 in Corsica on 14 Nov 2003; mainland France maintains a disease-free status), Spain (BTV 4 in Menorca island, Baleari, on 1618 Dec), Tunisia, Serbia
- 2004 : Spain, Portugal. BT entered Portugal and Spain for the 1st time in 1956 and reportedly persisted in Portugal until 1959, and in Spain until 1960, killing, within the 1st 4 months of the said outbreak, 46 000 sheep in Portugal and 133 000 in Spainref. The enormity of this outbreak was one of the reasons for the addition of BT to the OIE List A diseases. No additional clinical nor subclinical case of BT has been reported from (peninsular) Spain for the period from 1960 until October 2004, when (sub-clinical?) cases in bovines were detected. > 1000 cases have been reported, with 3,000 animals at risk within 142 separate outbreaks.
- joint or navel ill : generalized septicemia affecting foals, lambs, and calves, usually characterized by omphalophlebitis and the formation of abscesses in the joints resulting in polyarthritis; it is due to infection through the open navel by various organisms, including species of Staphylococcus, Streptococcus, Shigella, Escherichia, and Pasteurella, and has a high mortality rate
-
scrapie / cum tremblente
/ rida / traberkrankheit is a TSE
- UK : first reported in 1730. The government-funded Veterinary Laboratories Agency in Weybridge, Surrey, has confirmed that 83 "atypical" cases of scrapie have been found over the past 3 years in samples from 110 000 sheep brains tested from Ireland and UK. More worrying is the acknowledgement that of those 83 abnormal results, 12 have been found in sheep with the genotype normally associated with the highest degree of resistance to scrapie. The UK is obliged, under direction from the European Commission, to conduct brain tests each year on 10 000 sheep over 18 months of age which are processed in abattoirs, as well as a similar total which die on farms. Results have shown that only 0.3% of these sheep have been infected with scrapie, with many devoid of clinical symptoms. But it has been almost impossible to trace back the 83 "atypical" cases back to the farm of origin. This has prompted fears that the commission will insist the UK puts in place an individual identification scheme for sheep. This has been resisted by the UK on the grounds that no other member state runs sheep on an extensive regime such as in the Highlands and in the Welsh mountains, where stocking rates are very low. Tagging every lamb at birth and recording maternal details would be impossibleref.
- USA : it has infected > 1,000 flocks since its first detected case in 1947
- Japan : reported every year since 1996 to 2005, but it has not been reported elsewhere in Asia in the past 10 years. The Japanese are to be congratulated for their diligent reporting, since scrapie is recognized as occurring worldwide, with the exception of Australia and New Zealand.
- Italy : an accidental intra- and interspecies transmission of scrapie occurred in 1997 and 1998 following exposure to a vaccine against Mycoplasma agalactiae prepared on mammary gland and brain homogenates containing 2 prion strains.
- Norway : 5 cases of scrapie with unusual features have been diagnosed since 1998. The affected sheep showed neurological signs dominated by ataxia, and had the PrP genotypes homozygous A136 H154 Q171/ A136H154Q171 or heterozygous A136H154Q171/A136R154Q171, which are rarely associated with scrapie. Brain histopathology revealed neuropil vacuolisation essentially in the cerebellar and cerebral cortices; vacuolation was less prominent in the brainstem, and no lesions were observed at the level of the obex. The deposits of PrPSc were mainly in the cortex of the cerebellum and cerebrum, and no PrPSc was detectable by IHC or ELISA in the lymphoid tissues investigated. Western blot analysis showed that the glycotype was different from other known scrapie strains and from the BSE strain. From a diagnostic point of view, these features indicate that this type of scrapie, designated Nor98, could have been overlooked and may be of significance for sampling in scrapie surveillance programmes.
- Switzerland : a Nor98 case was reported in a farm with 12 sheep in Zurich canton : Switzerland last reported Scrapie in June of 1999
- Finland : reported for the first time in November 2002 (in a dairy herd of 44 goats and 6 sheep) and on 3 May 2004 (an 8 year old ewe, which was being treated for pregnancy toxaemia and died on the farm due to Nor98 type, in a flock comprising 27 sheep, in Oulu province (between latitude 64 deg and 66 deg North))
- Romania : first announced in 2003
- Slovakia : first announced in 2003
- Slovenia : first announced in 2004
- Norway
- France
- UK
- Switzerland
- Falkland Islands : on Oct 12, 2005, a 7 year old, home-bred ewe in a family farm of 4705 hectares, which has always bred naturally and has not been involved in any artificial insemination or embryo transfer program tested positive at Cape Dolphinref
- border disease of sheep : a highly fatal disease caused by a togavirus (pestivirus type 3), affecting sheep on the English-Welsh border, as well as in Australia and New Zealand (where it is called hairy shaker disease); it is manifested by increased hair in the fleece, slow growth, diminished stature, abnormal head shape, and a swaying gait.
- thin ewe syndrome : chronic caseous lymphadenitis in a ewe, with weight loss and reproductive failure.
- contagious agalactia : a contagious disease of goats and sheep in southern Europe and North Africa, usually caused by Mycoplasma agalactiae; symptoms include arthritis and eye lesions, with mastitis in females
- Clostridium perfringens type B => : a fatal enterotoxemia, usually seen in young animals, chiefly lambs, although it may affect sheep, goats, and cattle of any age. e toxin causes a rapidly lethal, acute toxemia in sheep primarily but also in other herbivores such as goats and cattle. Eating habits appear to be particularly relevant as an introduction of a diet containing protein and energy-rich foods as what may occur with fast growing young animals is associated with increased susceptibility. The "overeating" disease may be caused by undigested, starch ladened (high carbohydrate) food reaching the intestines where spores are better able to germinate and produce the prototoxin which undergoes protease digestion into the active toxin, the gene for which has been cloned in E. coli. The toxin causes an increase in intestinal permeability and some enteritis, producing toxemia, pulmonary edema, pericardial effusions, and swollen hyperemic kidneys ("pulpy kidney disease" : kidneys are mottled and soft in consistency and the cortex is jelly-like or almost semifluid) : liver is severely congested with small hemorrhages diffusely scattered over its surface. CNS disease is reflected by nervousness in sheep and less commonly as seizures or loss of consciousness. Cattle and older sheep are more likely to demonstrate neurological signs, and goats manifest more diarrhea. Cerebral edema in toxin-exposed animals appears to be a stimulus for the release of catecholamines and secondarily adenyl cyclase. In calves and adult goats, subacute nonfatal cases occur. Intravenous injection of e toxin in calves produces similar histopathological changes seen in sheep and goats after enteric exposure including acute pulmonary edema and cerebral edema. Delivered to humans as an aerosol in adequate doses, it is thought that the toxin could initially cause pulmonary edema with the possibility of secondary kidney, cardiac, and nervous system damage. As with staphylococcal enterotoxin B disease, the doses of e toxin possible to be delivered would result in debilitation of military or civilian populations rather than death. Although not specifically listed as a agent of biological warfare, C. perfringens a toxin (a potent phospholipase), when aerosolized, to cause severe, lethal pulmonary disease in animals due to a pulmonary capillary leak resulting in ARDS. Absorbed a toxin could lead to intravascular hemolysis, thrombocytopenia, and liver damage
- Nairobi sheep disease : an infectious disease of sheep and goats in East Africa, marked by acute hemorrhagic gastroenteritis, green, watery diarrhea, mucopurulent nasal discharge, and breathing difficulty; it is caused by a bunyavirus transmitted by the ticks Rhipicephalus appendiculatus and Amblyomma variegatum
- pregnancy toxemia in ewes / twin-lamb disease / lambing paralysis : an acute disorder in ewes caused by ketosis during the last few weeks of pregnancy, especially when they are carrying twins, triplets, or a large single lamb; the usual cause is undernutrition associated with stress. It can lead to impaired nervous function, coma, and death
- redfoot / red foot : a fatal condition of unknown etiology affecting newborn lambs, in which the sensitive lamina of the feet become exposed owing to detachment of the overlying horn.
- tribulosis : poisoning in sheep in South Africa caused by eating wilted plants of the species Tribulus terrestris; symptoms include hepatic injury, photosensitization, and encephalopathy .
- sheep and goat pox : an acute to chronic disease of sheep and goats characterized by generalized pox lesions throughout the skin and mucous membranes, a persistent fever, lymphadenitis, and often a focal viral pneumonia, with lesions distributed uniformly throughout the lungs. Subclinical cases may occur. Differential diagnoses include bluetongue, PPR or Kata, contagious ecythema, photosensitisation, insect bites, parasitic pneumonia, and mange
- ovine babesiosis : infection in sheep and goats transmitted to mammals by tick vectors. Symptoms include jaundice and hematuria
- Babesia motasi (usually more severe) : a species infecting sheep and goats in parts of Europe, the Middle East, Indochina, Northern Africa, and the former Soviet Union, transmitted by the ticks Rhipicephalus bursa, Dermacentor sylvarum, and Haemaphysalis punctata.
-
Babesia
ovis : a species infecting sheep and goats in the tropics and in
southern Europe, the former Soviet Union, and the Middle East, transmitted
by the ticks
Rhipicephalus
bursa and Ixodes
persulcatus.
- Rupicapra
-
Rupicapra
rupicapra (chamois) : orf
virus / contagious pustular dermatitis virus / ecthyma contagiosum virus
- Rupicapra pyrenaica pyrenaica (a.k.a. Pyrenean chamois, rebecos in Spanish, known locally as sarrio and isard) is a free-living ruminant grazing with domesticated cattle and sheep in the Pyrenean mountains, with a population of about 25 000 animals. Pestiviruses (family Flaviviridae) affect ruminants and suids. There are 4 accepted pestivirus species: Border disease virus (BDV), Bovine viral diarrhea virus-1 (BVDV-1), BVDV-2, and Classical swine fever virus (CSFV). According to 2 research groups (see further), a pestivirus, closely related to Border disease virus, has been isolated from affected chamois. Border disease (BD) is a transmissible congenital disease caused by a pestivirus that affects sheep and occasionally goats. The disease has been recognized in most sheep-rearing areas of the world. Clinically, BD is characterized in sheep by abortion, stillbirth and the birth of weak lambs with nervous disorders. The BD virus induces, under some conditions, a severe hemorrhagic syndrome; this hemorrhagic disease was reported in 1983 in the Aveyron department (southern France). The isolation of a BDV-like pestivirus, by itself, is not sufficient to incriminate this virus for the death among Pyrenean chamois; to establish its role as the causative agent, the requirements of Koch's Postulates should be fulfilled: the disease has to be experimentally reproduced. A high pestivirus prevalence was also found in Italian chamois too; also a possible new strainref. Contrary to the observations from the Pyrenees, this paper does not mention observed clinical problems or increased mortality in Italian Chamois. The goal of the study was to investigate seroprevalence of pestivirus in 4 alpine wild ungulates in the High Valley of Susa, north-west Italy: red deer (Cervus elaphus), roe deer (Capreolus capreolus), wild boar (Sus scrofa) and chamois (Rupicapra rupicapra). A further goal was using virus neutralisation tests (VNT) for 4 strains of pestivirus in chamois and wild boar. 375 serum samples collected during the hunting season of 1999 were tested for pestivirus-specific antibodies. Positive sera of chamois and wild boar were subsequently tested in a VNT with 4 major subtypes of pestivirus, and virus isolation was performed. No antibodies were found in the 73 samples of roe deer, while 7 (12.5%), 8 (5.9%) and 28 (25.5%) of 56, 136 and 110 samples of wild boar, red deer and chamois were ELISA-positive, respectively. Different ranges of titers were found in the VNT and no pestivirus was isolated in the ELISA-positive wild boar and chamois samples. Seroprevalence was particularly high in chamois. Further investigation is needed to characterise the pestiviruses that circulate in these animals.
- Hippotraginae
- Oryx
- Oryx dammah (scimitar-horned oryx)
- Oryx gazella (gemsbok)
- Oryx leucoryx (Arabian oryx)
- bowie : a disease resembling rickets that affects unweaned lambs in New Zealand
-
pasteurellosis in sheep and goats is caused by Pasteurella
spp.. Most often those are Mannheimia
haemolytica (a.k.a. Pasteurella haemolytica) and Pasteurella
multocida,
as these organisms are often commensal with the tonsils and nasopharynx
of healthy sheep and goats. These are nonmotile, non-spore-forming aerobic
gram-negative coccobacilli. There are 16 serotypes of P.haemolytica
that are currently recognized. As Pasteurella can survive for days
in moist secretions or water, close contact is not required for the infection
to pass from goats to big horn sheep; they merely have to graze the same
area within a few days of each other. It may be seem convenient to
blame the goats, but that may be because the connection is obvious, and
this doesn't make it any less likely. Generally, it is a respiratory disease,
but also manifests as septicemia, arthritis, meningitis & mastitis.
Pneumonic
pasteurellosis is caused most often by P. multocida in sheep
and goats and can lead to high mortality and great economic loss. Transition
from infection to disease appears to be facilitated by various stressors
including concurrent infections, changes in climate, pasture, or feed,
and other management factors
- Cervoidea
-
Cervidae
(deer) : Dermatophilus
congolensis,
Yersinia
pestis,
foot-and-mouth
disease virus (FMDV),
Mycobacterium
bovis
(TB can be transmitted in a number of fashions, including close or nose-to-nose
contact. TB is a disease that develops slowly, so it may be difficult to
know when and where these animals were exposed to the disease), Mycobacterium
avium subsp. paratuberculosis
(Johne's disease / chronic dysentery of cattle
/ paratuberculosis). In 2005 some 9-10 ranches in Sutton County,
USA have affected stock, mainly deer : it is claimed that there have been
no recorded cases of anthrax in the area in some 70 years. If that is true,
which I severely doubt, it would have to have been brought in, possibly
in latently infected replacement stock from a deer farm affected during
the 2001 epidemic. It is more likely that it has been happening all along
but the sporadic nature of scattered individual deaths allowed it to be
seen but not observed. All affected dead animals should be burnt. Last
summer the "British Barbecue" system of burning deer carcasses was
developed, which involves three 20-lb sacks of the cheapest charcoal briquettes
and a 10-lb bag; the 20-pounders go under the carcass, the 10-pounder under
the head after slicing open the paper sacks and adding diesel fuel. Place
the carcass on top and light carefully. This will effectively burn a deer
carcass in 60 minutes, which is cheaper (cost < USD 20), faster, and
quicker than cutting wood and piling up rubber tires. Obviously with more
dead deer efficiencies of scale can be obtained, which should bring the
cost down to USD 10/deer. It is called the British Barbecue to differentiate
it from the admirable Texas barbecue for cooking beef. With cows you must
get an airflow under the carcass if you want to burn it quickly, i.e. in
one day. This outbreak followed the classic Texas anthrax weather pattern
of wet weather followed by hot and dry; whether we will see a parallel
epidemic in Val Verde, Edwards, and Uvalde counties is not known but frankly
expected. Just as we might well see outbreaks in Jim Hogg County to the
south, where it is normally truly sporadic. Interestingly, the trigger
is a brief shower in this long hot weather with deer deaths following 10
days later. The explanation would be that the brief shower provides a brief
vegetative growth, especially in the already short dry grazing, and therefore
the consumption of spore contaminated-soil during grazing. White-tailed
deer are normally browsers but do graze. If one of this summer's hurricanes
were
to come ashore in south Texas, the resulting downpour inland would wash
off all the spores deposited on leaf browse by the blow flies after they
fed on infected carcasses. The onset of wet season rains normally terminates
anthrax outbreaks in the African parks, and logically the same scenario
should apply here.
- Cervinae
- Cervus
- Cervus dama (fallow deer)
- Cervus elaphus (elk)
- Cervus nippon
-
Cervus
nippon nippon (Japanese Sika deer) : Hepatitis
E virus (HEV)
- Odocoileinae
- Alces
- Alces alces
- Alces alces americana (a.k.a. American moose)
- Odocoileus
- Odocoileus hemionus (Colorado mule deer)
-
Odocoileus
virginianus (white-tailed deer) : Borrelia
burgdorferi
- Ozotoceros
-
Ozotoceros
bezoarticus (pampas deer) : Leptospira
interrogans
- Rangifer
=> in 1991, rinderpest was diagnosed in yaks in the former Soviet Union, near the border with Mongolia. At the peak of the epizootic, mortality among affected yaks was 32-42% in adults and 65% in animals less than one year old. However, if rinderpest is involved in the current yak die-off, it may be assumed that the typical diarrhea would not remain unnoticed, even if only dead animals were observed. Mortality in adult yaks could be ascribed to numerous etiological agents, both non-infectious (metabolic, toxic) and infectious ones. Among the possible infectious agents, various bacteria (e.g. anthrax and pasteurella), viruses, protozoa and helminths might be taken into considerations.
=> a male zoo animal born on 24 Jun 1985 in Basel, Switzerland died on 7 Apr 2004 of BSE on probably feed with meat-and-bone meal
Taenia saginata
,Otobius
megnini,
Hypoderma
bovis,
Babesia
bovis,
Babesia
divergens,
Dermatophilus
congolensis,
Bacillus anthracis
(bovine anthrax :
Epidemiology : contaminated muddy hay in a 'champs maudit' (a field with a history of repeated anthrax outbreaks) is not an unusual epidemiological history. Gravesites on the banks of various rivers and even at the bottom of artificial water reservoirs do not pose any serious epidemiological concern. A few years ago this happened in Oklahoma, but similar reports go back decades to the 1920s in France.
with the disease at a farm in Wrexham in 1989ref. The pattern of UK anthrax outbreaks in the past 25 years is essentially no longer from contaminated livestock feed --- the Wrexham pigs were a notable exception --- but usually occur following an environmental disturbance, such as trenching, bulldozing, or river dredging, disturbing buried spores at cattle grave sites or occur in relation to mills & tanneries that handled contaminated imported hair & hides. This is a common epidemiologic pattern once an area is considered to be in a true sporadic state epidemiologically. At one time the UK had some 425 outbreaks each year over the course of decades thanks to contaminated feed. Once this was cleaned up, the rate dropped precipitously to the present situation when years go by without cases. It is now frankly a rare event subject to specific trigger events and as time goes by, it will potentially become even rarer, as spores are not immortal and can also lose their plasmids over time. Otherwise we would be vaccinating cattle annually in Europe & North America. We don't. And we have a situation where livestock veterinarians are ignorant of the disease (not having seen much of it during their careers), which delays recognition. This is further exaggerated in the UK where far too many farmers are now too poor to regularly employ a veterinarian. This Welsh outbreak is a good example as 5 cows had to die before it was diagnosed. I am mildly puzzled at the timing. April is early for this disease in the UK for it to be due to environmental exposure; theoretically dirty feed is available year round. But without details one can only muse about possible sources. And before anyone comes up with claims of Lazarus spores, my colleague & good friend Peter Turnbull once investigated an outbreak in Dorset, southern England, where some 5-6 steers were affected from a cow buried some 60 plus years previously; Peter located the grave in the pasture and showed the presence of viable spores in the surface soil
Prevention :
(bovine brucellosis : it is endemic in Korea; 110 outbreaks have
been reported during 2002. Brucella abortus had not been isolated
from any premises in Great Britain since October 1993 until its confirmation
on 4 premises in Scotland during early 2003. An additional, unrelated case
was identified later (2 Dec 2003) in a Scottish beef herd when post-import
blood testing was undertaken on a heifer imported from the Republic of
Ireland. All the infected and contact cattle at risk of infection were
slaughtered. Reportedly, all 4 outbreaks were caused by the importation
of infected cattle. In March 2004, a whole breeding beef herd was slaughtered
in Cornwall on the strength of a Brucella abortus biovar 1 isolate
from an
aborting cow. 3 other cows aborted with culture-positive vaginal swabs or fetal stomach contents. A specialist epidemiological team was set up to look into the source of the infection. The results of the said investigation were published by DEFRA on 20 Jul 2004 (press release 287/04). The conclusion was that the infection had, most likely, been introduced into the herd in Cornwall between Spring 2002 and Spring 2003 and that it was an isolated incident. The origin of infection was never identified, for which 2 reasons were offered:
,
Escherichia coli O157:H7
Prevention : vaccine administered in 3 doses at 3-wk interval. Both the Bioniche Life Sciences Inc. manufactured vaccine and the vaccine produced by the Alberta Research Council - Biologics fermentation facility demonstrated significant effectiveness and the most effective commercial-vaccine formulation resulted in a 99.56% or 2.35 log reduction in the amount of bacteria shed in manure, and a 70% reduction in the number of animals shedding after a single, orally-administered challenge with 1x109 or one billion E. coli O157:H7 bacteria 2 weeks following the last vaccination
Coxiella burnetii
,
Leptospira
interrogans serovar hardjo,
Anaplasma
phagocytophilum,
Chlamydiophila psittaci
(Buss disease / sporadic bovine encephalomyelitis : encephalomyelitis
with pleuritis affecting cattle in the United States, Japan, and parts
of Europe; characteristics include fever, labored breathing, cough, diarrhea,
and neurological signs such as a staggering gait; sometimes there is drooling
or a nasal discharge),
bovine papular stomatitis virus
,
Crimean-Congo hemorrhagic fever virus
,
Rift Valley fever virus
(adult cattle are known to be less susceptible than young animals; less
susceptible than sheep),
Wesselsbron virus (WSL)
(Wesselsbron disease : a viral disease of sheep and cattle in southern
Africa, resembling Rift Valley fever but caused by a flavivirus. It causes
death in newborn lambs and abortion in cows and ewes; human infection results
in mild febrile illness), rabies
virus
(vaccinations should especially be done in animals being prepared for show,
primarily because of the much closer, more frequent contact with people),
foot-and-mouth
disease virus (FMDV)
(foot-and-mouth disease (FMD) / aftosa / aphthous fever / hoof-and-mouth
disease / contagious or epizootic aphthae / tabak (in Pakistan) : an
acute extremely contagious disease caused by a picornavirus, affecting
wild and domestic animals, particularly ruminants and pigs, and occasionally
humans
=> epizootic aphta / aphthous fever / foot-and-mouth disease (FMD) / illness No.5 : acute fever, followed by the eruption of vesicles on the lips, buccal cavity, pharynx, legs, and feet; sometimes the skin of the udder or teats is involved. Infected animals secrete numerous virus particles before clinical signs appear; infected cattle become weak and yield less milk. Though it is true that animals can survive FMD, production drops dramatically. Certain strains of the O serotype may be even more infective and invasive than Asia 1 serotype, affecting several susceptible species
Epidemiology :
No / report date / infected species / location (province)
Laboratory examinations : the tissue of choice is epithelium. Ideally, at least 1 g of epithelial tissue should be collected from an unruptured or recently ruptured vesicle. Where epithelial tissue is not available from ruminant animals, for example in advanced or convalescent cases, or where infection is suspected in the absence of clinical signs, samples of OP fluid can be collected by means of a probang (sputum) cupref. These tests may occasionally give false positives, mainly in older animals with a history of regular repeated vaccinations. A negative result for antibody to NS proteins cannot be taken as definitive proof that an individual animal has not been exposed to FMD virus. This must be taken into account if NS protein antibody tests are used for assessment of risks for animals involved in international trade. Anyway an ELISA test looking for antibodies recognizing strain-independent infection-specific linear B-cell epitopes located in the nonstructural (NS) proteins has been recently developed to differentiate between infected and vaccinated cattle. However, an issue not yet solved is the identification of "carrier" animals, which can be produced by vaccination and consecutive infection. These animals without FMDV symptoms are a continuous threat for nonvaccinated animal populations. A sensitive method for detection of these animals is highly important for FMDV diagnosis; the author say that detailed analyses of carrier animals and their antibody repertoire will be the subjects of further studies.
Prognosis : left alone, adult animals recover within weeks.
Prevention : the animal vaccineref takes 7 days to be effective, hence IFN-a
has to be used in the meanwhile.
Generally meat from FMD infected animals -- with thorough cooking -- is considered safe for consumption. But transporting the animal to the processing plant may spread the disease, which is why most infected animals are not transported to a processing plant. Routine vaccination against FMD is done on a regular basis in Egypt using locally manufactured oily dead virus vaccine against FMD serotype O1. Vaccination by bivalent strains of FMD (A and O) will be undertaken. Some countries in the Middle East have been applying annual vaccinations with a trivalent vaccine, including the serotypes O1, A22 and Asia 1. It is not clear whether these vaccines will protect against the Egyptian strain. The genotyping of the Egyptian FMD A virus, and its relationship to vaccine strains currently in use within the region, such as <A22 Iraq 87> and <A Iran 96>, are urgently required. Samples from Egypt were tested by the World FMD Reference laboratory WRL at Pirbright. The results were included in the February 2006 report: the strains, EGY 1/2006 Cattle 09.02.06 and EGY 2/2006 Cattle 09.02.06, were found to be serotype Aref. No additional data on the said strains, with special reference to their genotyping, could be found on the WRL's website. Their relations to other FMD A genotypes -- particularly potential vaccine strains -- are of importance. Such data, and provision of seed material of the candidate vaccine strains, are needed urgently for the selection and production of efficient vaccines to prevent further spread in Egypt and elsewhere. In the past, the Middle East witnessed major FMD pandemics which spread throughout the entire region and, in several occasions, reached southeastern Europe
Web resources : The OIE/FAO-designated World Reference Laboratory for FMD (WRLFMD)
..., Vesicular stomatitis virus (VSV)
- Transmission :
- Feeding of ruminant derived protein to ruminant
animals has been forbidden in UK in July 1988 (in Canada in 1997): PAPs
are better detected with immunoassays than with PCR.
- Surveys conducted by USDA place the number of
downer cattle (those that have trouble walking to the slaughterhouse under
their own power) at between 150 000 and 200 000 animals annually. Downer
cows does not mean diseased cows. It means the animal cannot get up, because
of a torn tendon, perhaps from a rough trailer ride, or a broken bone from
a slippery floor. There are reasons that animals can fall, and can be injured.
It does not mean they have a neurological disease. Other reasons for "downer
cattle" include having a large calf, which can injure the obturator nerve
as the calf squeezes through the birth canal. Though neurological disease
is not a factor in the ratio of the size of the calf vs that of the birthing
canal, a downer cow is the result. This is not brain-related neurological
disease any more than if a severed spinal cord on an athlete resulted from
a throw from his polo pony. Whatever the reason the animal is down, this
status now means this animal will not be allowed into the human food chain.
Those downers will still be used for pet food and other products, including
tallow and cosmetic ingredients [There certainly is nothing more than speculation
at the moment as to what the downed animals may go for. However, these
cows are not likely to be used for pet food. The final rules are not yet
complete, but many of the pet food manufacturers do not want downer animals,
because they want to be assured of the safety of the pet food, and because
some indigent people consume pet food.]. Affected animals will no longer
be going to slaughterhouses but instead most likely most of them will be
euthanized and sent to rendering plants, whose products fall within
2 major categories :
- Rendered products are not found in baby food products, aside from possibly
fats (lards), which are inspected for safety and cleanliness by the FSIS.
Specified
risk materials / specified bovine offals (SBO) whose use in the human
food supply and advanced meat recovery (AMR) (an industrial technology
developed a decade ago that uses hydraulic pressure to force extra pounds
muscle tissue from the bone of cow carcasses, without incorporating bone
material when operated properly, producing filler for processed foods like
hamburger, hot dogs, and pizza toppings. Consumer groups initially complained
that bone was getting into the advanced meat recovery product and argued
that the product should not be labeled as beef. Then, in 1997, federal
agriculture officials announced that they had found spinal cord tissue
in some of the meat) is prohibited by USDA include skull, brain, trigeminal
ganglia, eyes, vertebral column, spinal cord, and dorsal root ganglia (DRT)
of cattle over 30 months of age, and tonsils and small intestine of cattle
of all ages. The 1997 ruminant-to-ruminant feeding ban was changed in Dec
2003 to a mammalian-to-ruminant feeding ban, which means that no
mammalian tissue can be processed and fed to ruminant animals (cattle,
goats, and sheep). The use of these animals as feed for birds, specifically
commercial poultry (chickens and turkeys) has caused some concern. Poultry
litter is often fed back to cattle, and the concern is that any prion may
pass through the litter and be transmitted to the ruminant animal. There
is little concern that birds are susceptible to prion agents : although
genetically modified chickens have been made to produce the disease under
experimental conditions, it is not found naturally. Likewise, the issue
of fish being susceptible to prion disease has not been proven in the natural
setting, and is again of little concern. One must understand that feed
manufactures and renderers are not the same. Renderers produce a starting
material that is delivered to the feed manufactures. Feed manufactures
include a variety of livestock feed manufacturers as well as pet food manufacturers.
Meat and bone meal is still an acceptable product to be fed to companion
animals. To ensure that portions of the brain are not dislocated into the
tissues of the carcass as a consequence of humanely stunning cattle during
the slaughter process, FSIS is issuing a regulation to ban the practice
of air-injection stunning. USDA will prohibit use of mechanically separated
meat in human food. In June 2006 cattle tissue may have contaminated 2
feed ingredients given to dairy cows -- Pro-Lak and Pro-Amino II -- made
by H.J. Baker between August 2005 and June 2006. The 3rd of the recalled
ingredients, Pro-Pak with Porcine Meat and Bone, was mislabeled. It is
used in poultry feedref.
The methodology by which the Geographical BSE Risk (GBR) of countries is assessed was developed by the Scientific Steering Committee (SSC) of the EU as a qualitative indicator for the likelihood of BSE being present in the relevant countries, basically trying to answer 2 questions:
OIE defines a minimal risk country as having had < 2 cases per million cattle over the age of 24 months.
The reclassifications of Canada and the USA, from GBR category II ("unlikely but not excluded") to category III ("presence of BSE likely but not confirmed, or confirmed at a lower level"), were inevitable since the detection of their 1st BSE cases. Norway's reclassification from "highly unlikely" to "unlikely but not excluded" means its exporters will have to remove more of the "significant risk material (SRM)" before shipping beef into the EU. GBR re-assessments of Botswana, Costa Rica, El Salvador, Nicaragua, Namibia, Panama and Swaziland, presently classified in level I, are expected before the end of 2004.
(*) 100% testing of healthy slaughtered animals
(**) 100% testing up to 100
Compared to 184,005 BSE cases recorded in the UK so far, 5003 cases have
been recorded in the 23 other -- mostly European -- countries.
Cases in born after ban (BAB) animal are a matter of concern, but are not solitary and should not be overly surprising. The final, total, and effective feed ban ("real ban") in the UK was implemented since July 1996. However, according to Defra's statistics as of 1 Jun 2004, the number of confirmed born after real ban (BARB) cases has been the following (year of birth): 1997: 35; 1998: 19; 1999: 7. BSE-positive cases recorded between July 2001 and November 2002 in European risk stock born during 1997-1999ref; in brackets: rate per 1 million adult cattle:
During 2003, decreased incidence of recorded BSE cases, compared to 2002, was seen in most countries. The exceptions were Portugal, Spain (with a relatively high number of cases), Japan, Poland, and the Czech Republic. The 3 countries with the highest ratio of BSE-positive risk animals per 10 000 animals tested are Portugal (23.11), UK (18.40), and Ireland (12.81). In all 14 BSE-affected states except Portugal, the ratio decreased during 2003 compared to 2002. Greece has a very low testing rate. Being one of the 3 countries which have so far recorded only one BSE case (all 3 in 2001), out of the 14 affected states (Sweden is still BSE-free), it is interesting to compare Greece to the other 2 countries in this exclusive group, Austria and Finland. The testing rate in risk animals (percentage of adult animals in national herd) during 2003 was: Finland, 5.86 (the highest of all 15 states); Austria, 1.75; Greece, 0.62 (the lowest of all 15 states). It seems that Greece's claim to the absence of BSE cases since 2001 will be fortified by enhanced testing efforts, especially in risk animals. The same observation might be valid in respect to Greece's testing of healthy animals: during 2003, the mean percentage of tested healthy animals in the 14 BSE-affected EU states was 22.4, while Greece tested only 7.5% of its adult cattle.
During 2004 as previously, the 2 countries with the highest annual BSE incidence rate in 2004 were Portugal (93.870) and the UK (67.796). 4 countries have experienced in 2004 an increased incidence rate compared to the previous year, namely Slovakia, Poland, the Czech Republic and Japan (in descending order). Though Germany experienced also an increase, its calculated incidence rate has not yet been included in the OIE table.
It can take from 20 months to 15 years for an animal to exhibit infectious prions in its brain stem after eating infected feed : no one knows whether prions accumulate in small amounts in other issues early on, and current tests are devised to find them only in the brain stem.
In the USA, even under the new rules, testing will be quite limited, restricted almost exclusively to downed cattle. In the last 13 years, the USDA has tested about 57 000 animals out of about 390 million slaughtered. In 2003, it tested 20 526 cattle out of 35 million killed. The tests were done on brain samples at the Veterinary Laboratory in Ames, Iowa (National Veterinary Services Laboratory, NVSL). The testing method they use, which takes a week, is based on IHC. In contrast, European countries use 5 approved tests to screen a million cattle a month -- 1 of every 4 brought to slaughter. No tests are used on muscle meat or other body parts. The result is that France, for example, tests more cattle in a week than the US has tested in a decade. Most countries test animals over 30 months of age, but several, including Britain, test at or above 24 months. The rationale for testing older animals is that prions are thought to take 3 to 5 years to reach the brain, although that has never been proved. In all, European nations tested 19 million cattle in 2003 and found 4200 cases of BSE, mostly in older cows. But several younger animals, one only 20 months old, have been diagnosed with the disease in recent years in Japan, England, and Slovakia. Animals to be tested are killed and their carcasses held in refrigerated warehouses overnight. Brain stem tissue, where prions are usually 1st found, is sent to a lab for testing. The diagnosis is sent to the slaughterhouse the next day. Infected animals are culled and incinerated or buried in special landfills. In Japan, every cow headed for the dinner table is tested for the disease. Since testing began 3 years ago, only 9 out of 1.2 million cattle that have been tested per year were diagnosed with mad cow disease. The youngest was 21 months old. There is also a question of which tissue to test. We don't know where and how prions move through the body before they show up in the brain, but there is a way to find out. The test would be to infect calves, kill them at different ages, remove at least a dozen types of organ tissues -- including muscle, heart, and kidney -- and place those tissues into mice engineered to have the normal cow prion. If any mice get sick, it would be possible to pinpoint where the infection exists outside the brain. Although that experiment has not been done yet, a similar experiment has been completed in the UK. The prions were given to calves (via feeding, not via intracranial injection); the animals were sequentially killed at various times and a variety of organs examined at each time pointref. So although the work has not been done in mice, it has been done in cattle, which -- of course -- are a better model for a cattle disease than mice. The experiment took about 6 years and has not been repeated, but was considered to be substantial work. Bovines born in Autumn are 100-fold more likely to develop BSE than animals born in Spring. Bovine PrPSc can be transmitted to humans, Ovis aries and Capra hircus. In 1996 the Food Standards Agency introduced the Over Thirty Month (OTM) banning meat from most cattle aged over 30 months from being sold for human consumption.
Atypical isoforms :
in humansref.
Their unusual strain was discovered only because Italy tests all cattle
over 24 months old slaughtered for human food (Italy modified the application
of Regulation (EC) No 999/2001 of the European Parliament and of the Council
of 22 May 2001, laying down rules for the prevention, control, and eradication
of certain transmissible spongiform encephalopathies (amended by Regulation
(EC) No 1248/2001 of 22 Jun 2001), with Law-Decree No. 344 of 4 Sep 2001,
in which the age for testing healthy cattle, including buffalo and bison
slaughtered for human consumption, was lowered to 24 months. Examination
of dead animals not slaughtered for human consumption, having died on the
farm or during transport (fallen-stock), like examination of animals subject
to "special emergency slaughtering", was already established at 24 months
by EC Regulation). By August 2003, it had tested 1.6 million and found
103 that tested positive for prions- It has been estimated that the non-vegetarian component of the UK population
(say some 40 million people) consumed at least 50 meat-containing meals
per person during the course of the BSE epidemic. As of the end of 2003
the number of confirmed vCJD cases stands at only 145, the precise mode
of transmission of the BSE prion to humans has been difficult to establish
unequivocally, particularly because at least one of the confirmed cases
was a person of predominantly vegetarian habit. A hereditary component
in susceptibility to vCJD is evident from the observation that so far all
confirmed cases of vCJD exhibit a met/met genotype at codon 129 of the
common prion protein gene (PRNP). It is unclear whether val/val homozygotes
or met/val heterozygotes are indeed resistant to development of vCJD, or
whether the met/met genotype merely predisposes individuals to early onset
vCJD. For this reason it may be premature to conclude that the vCJD outbreak
in the UK has now passed its peak. Data are limited but there are
indications that the frequency of the met/met genotype (and by inference
susceptibility to vCJD) may differ indifferent populations. In the Finnish
population the genotype frequencies of the PRNP codon 129 polymorphism
are homogeneous and do not differ by age or genderref.
Comparison of Finnish, British and Irish blood donors reveals distinct
differences in allele frequencies. The Finnish sample is 49% met/met, 42%
met/val and 9% val/val. By contrast the British blood donors are 42% met/met,
47% met/val and 11%t val/val, and the Irish blood donors are 34% met/met,
56% met/val and 10% val/valbacterial keratinase produced by Bacillus
licheniformis strain PWD-1 degrades PrPSc from infected
cattle and sheep. Only in the presence of detergents does heat pretreatment
at >100°C allow the extensive enzymatic breakdown of PrPSc
to a state where it is immunochemically undetectable. Proteinase K and
2 other subtilisin proteases, but not trypsin and pepsin, are also effectiveref
3 principal questions remain unresolved: the origin of the BSE epidemic; the future of vCJD; and what to do with the 16 million tonnes of animal byproducts produced annually by the slaughter industry. Loss of value and cost of disposal of MBM exceed 1.5 billion € [USD 1.8 billion] per year. Though new EU legislation could permit > 80% of this material to be used again in livestock feeds, the best option is to continue the ban on its use. The cost of the epidemic has been enormous, and is estimated here at about 10% of the annual output value of the European beef sector. The discounted present value of these costs is estimated at 92 billion € [USD 111 billion]. The progress of the epidemic was marked by many deficiencies and failures, of which 2 are particularly noted:
At the press conference held on May 27 2005 at the 73rd General Session, the Director General of the World Organisation for Animal Health (OIE), Dr Bernard Vallat, accompanied by the President of the OIE, Dr Niang, and by the President of the OIE Code Commission, Dr Alex Thiermann, gave some indications as to certain specific issues that were discussed and adopted by the 167 Member Countries and which are of particular interest for the public at large. These relate in particular to the following:
Prevention : Chinese scientists have succeeded in cloning a cow with gene cells resistant to mad cow disease. The birth of the 55kg calf in the eastern province of Shandong comes three years after a team led by now-disgraced South Korean scientist Hwang Woo-suk cloned cows with a protein structure resistant to BSE. Scientists with the Laiyang Agro-Science Institute in Shandong used gene-transplant technology to introduce the genes to the calf cloned from cells of an adult cow. The research was led by professors Dong Yajuan and Bo Xuejin - who succeeded in cloning China's first and second healthy cows in 2001 - in collaboration with a Japanese universityref
Web resources :
Epidemiology : until 1988 LSD was confined to sub-Saharan Africa (endemic in Zambia), but then spread into Egypt, Madagascar and Kuwait. There has been only one laboratory-confirmed outbreak of LSD outside Africa, in Israel in 1989, which was eliminated by slaughter of all infected and in-contact cattle, and vaccination. Outbreaks reported in Bahrain and Reunion in 1993 were not confirmed by virus isolation. Mauritius outbreak in 2000 was due to importation of cattle from a country on the African continent : 178 clinical cases were recorded, of which 2 animals died. The outbreak was eradicated by application of slaughter policy followed by general vaccination. No cases have been reported during 2001-2003. Table-form data on the incidence of LSD since 1996 is available on OIE web-site (Handistatus)ref; all affected countries are located in South Saharan Africa. There are scattered reports of LSD in the Middle East - Oman in 1984; Bahrain in 1993 and 2002-2003; Kuwait in 1991, and UAE in 2000. But the disease is regularly reported throughout Africa including Egypt in 2006 and 1990; regularly from Eritrea, Ethiopia, Somalia, and Sudan in 2003. LSD is also commonly reported from other parts of Africa. LSD antibodies had been detected in the serum of Arabian oryx (Oryx leucoryx) at the National Wildlife Research Centre in Taif, Saudi Arabia, collected as far back as 1987. A full-blown clinical case of LSD was diagnosed and documented in our centre in a captive-bred female Arabian oryx in 1991. Transmission from local livestock -- sheep, goats and camels -- was strongly suspected and vector transmission by arthropods fully considered, though never proven. The said female oryx aborted but was negative for endemic abortion-inducing diseases such as Brucellosis and Q fever. A serological test for LSD, carried out in a subset of the same animal group about 5 years later, was negative for LSD).
Transmission predominantly by insects, natural contact transmission in the absence of insect vectors being inefficient. LSD may occur in sheep and goats and has been transmitted from sheep to cattleref. It is generally agreed that LSD virus is host-specific. LSD is caused by strains of capripoxvirus that are antigenically indistinguishable from strains causing sheep pox and goat pox, though LSD has a different geographical distribution to sheep and goat pox, suggesting that cattle strains of capripoxvirus do not infect and transmit between sheep and goats.
Symptoms & signs : fever; 1-7 cm nodules on the skin and sometimes in the mucous membranesref and internal organs; emaciation; enlarged lymph nodes; edema of the skin; which may result in permanent sterility or sometimes death. It has a rather lengthy course and does not include diarrhea as a typical symptom. Morbidity can range from 3 to 85%, while mortality rates usually do not exceed 20%. It resembles dermopathic herpesvirus disease.
Prevention : in Egypt 2,105,887 bovines were given mandatory vaccination during 2004. For further information, the reader is referred to chapter 2.1.7 of OIE's Manual of Diagnostic Tests and Vaccines for Terrestrial Animalsref
=> infectious bovine rhinotracheitis (IBR) : an acute, infectious, febrile, disease of cattle, marked by inflammation and ulceration of the upper respiratory tract, which may be followed by pneumonia, coughing, profuse (muco)purulent discharge from the eyes and nose, excessive salivation, depression, anorexia, reduced milk yield and, in pregnant cows, abortion. IBR, generally a disease of cattle, is one of the differentials for clinical signs that may be seen in animals suspected of having foot and mouth disease. There are laboratory tests to distinguish between them. IBR is an OIE List B disease commonly evidenced either clinically or serologically in most European and many American countries. Mortality is low. Many infections run a subclinical course. Secondary bacterial infections can lead to more severe respiratory disease.
=> infectious pustular vulvovaginitis (IPV) or balanoposthitis
Transmission : ticks Amblyomma hebraeum and A. variegata
=> heartwater / cowdriosis / veld or veldt disease or sickness : a fatal rickettsial disease of cattle, sheep, and goats in sub-Saharan Africa and on certain islands in the Indian Ocean and the Caribbean (where it poses a threat of spreading to the American mainland), marked by fluid accumulation in the pleura, pericardium, and pleural cavity
The current "vaccine", infective sheep blood, involves infection of the animals to be vaccinated with live organisms followed by treatment with antibiotics. There are a number of drawbacks with such a vaccine strategy and there is an urgent need for a new and improved vaccine.
Epidemiology :
Hungary : a sheep aged > 5 yrs-old originating from Romania for immediate slaughter in December 2004 tested positive at rapid test on Dec 16 and test was repeated on samples from the obex and the cerebellum. On May 2006 2 fatal cases occurred in sheep on a farm in Sakeresztur (46°98'27" N by 18°55'46" E) in Fejer countyref
Transmission : through amniotic fluid, so infected ewes easily pass the illness to their lambs
Symptoms & signs : severe itching that makes animals scrape themselves against trees and fences (hence the name), (paresthesia ? who can say it ?), muscular incoordination, tremors, stumbling gait, and eventually, lethargy, increasing debility, ending in death.
Pathogenesis : in May 2004 a study team, based at 3 French research institutes, found prions in the leg muscles of sheep that were naturally infected with scrapie and in sheep deliberately infected with it at 1/5000 the concentrations that are found in sheep brains, and therefore likely to be much less infectious : no case of scrapie transmitted to humans has ever been found and no researcher has ever infected a healthy animal with a prion disease by injecting it with liquefied muscle from a sick one -- not even when the injection was directly into the brain. It is even less likely that a human could be infected by lamb or mutton that has passed through the acidic process of digestion. In one naturally infected sheep, they found scrapie 8 months before the animal showed any signs of the disease. Prions have been found in the muscles of infected humans and rodents but not previously in the muscle tissues of animals whose meat is commonly eaten by people. In the last few years, the sensitivity of immunoblot tests has been ramped up so much that people are beginning to find the protein all over the place. BSE appears to have a much more restricted tissue dissemination and reduced involvement of the lymphoreticular system in comparison to scrapie in sheep. The prominent organs found with infectivity in cattle were the brain, spinal cord, dorsal root ganglia, trigeminal ganglia, distal ileum, and bone marrow. Until recently, it was generally agreedref that the highest levels of infectivity in sheep were recorded in brain and spinal cord; moderate levels -- in various lymph nodes, spleen, tonsil, ileum, proximal colon, and peripheral nerves; low levels were recorded in cerebral spinal fluid, nasal mucosa, adrenal glands, sciatic nerve, distal colon, pancreas, liver, bone marrow, thymus, and supramammary lymph node. No detectable infectivity was reported in blood clot, mandibular and parotid salivary glands, thyroid, heart, lung, kidney, mammary gland, and testis. Experimentally and naturally scrapie-affected sheep accumulate the prion protein PrPSc in a myocyte subset. In naturally infected sheep, PrPSc is detectable in muscle several months before clinical disease onset : the relative amounts of PrPSc suggest a 5,000-fold lower infectivity for muscle as compared to brainref.
Atypical cases of scrapie have been reported, since 2003, from :
Web resources : Organismo
Internacional Regional de Sanidad Agropecuaria (OIRSA)
=> in the 1960s, a parasitic nematode, Parelaphostrongylus tenuis ("meningeal worm", also "deer worm"), was reported as constituting a probable explanation for a wasting, debilitating disease with uncertain aetiology affecting moose in Eastern North America. Several clinical and pathological signs remained unexplained. Recently, a similar syndrome in Nova Scotia moose has been found by A. Frank et al to be related to cobalt and vitamin B12 deficiencyref
=> chronic wasting disease (CWD) / mad-deer disease is a TSE
of
...
Clinical signs include lethargy, drooping head or
ears, tremors, stumbling, excessive salivation, difficulty swallowing or
excessive thirst or urination, loss of wariness of predators and slowly
deteriorating body condition. The disease is always fatal and there is
no known cure or treatment to prevent CWD. Because deer and elk show signs
of disease much earlier in lymph tissue, samples can be obtained in live
animals from tonsil biopsies. In an experimental herd in Colorado,
some 90% of animals succumbed to the disease within 4 years, regardless
of whether their parents were infected or not. It is not known how the
disease arose in the captive animals : in the wild, where deer do not live
in such close proximity, CWD spreads more slowly. The disease can pass
between unrelated animals in urine, saliva or faeces, via routes such as
shared scratching posts or grazing land contaminated by whole carcasses
or excrement of infected animalsref,
and from mother to unborn fawn : deer are just as likely to catch the disease
from one another as they are from their motherref.
At present, up to 10% of Colorado's 500,000 mule deer carry the disease.
CWD was 1st recognized in 1967 in Colorado, and it subsequently was found
in captive herds in 9 states and in 2 Canadian provinces and in free-ranging
deer or elk in 9 states and one provinceSince its first appearance in Colorado
in 1967, the disease has spread across 12 states : the disease has been
found in Minnesota, Montana, Kansas, and Oklahoma in captive animals and
in wild, free-ranging deer and elk in northeastern Colorado, southeastern
Wyoming, Nebraska, South Dakota, Wisconsin (on 28 Feb 2002, the 1st cases
of CWD were reported for 3 deer near the city of Mount Horeb in south-central
Wisconsin), northern Illinois (in the past 2.5 years there have been 54
cases in the state from 4 counties: Boone, Winnebago, McHenry, and 4 in
DeKalb), Utah, southern New Mexico (12 wild deer and 2 wild elk since 2002,
when the disease was first discovered near the eastern foothills of the
Organ Mountainsref1,
ref2,
ref3,
ref4,
east of Las Cruces. All of the CWD-positive deer and elk in New Mexico
were from the southern Sacramento Mountains southeast of Cloudcroft and
areas surrounding the Organ Mountains near Las Cruces), and New York State
(first 2 cases on Mar 2005 in 2.5- and 6-year-old white-tailed deers from
a captive herd in Oneida County) USA. The New Mexico site being close to
Texas and to Mexico has spawned speculation, but as yet without foundation
: in the past 3 years Texas has tested some 9103 deer out of a target population
estimate of 3 917 926, all negativeref1,
ref2.
In Wisconsin, based on testing the past 2 years, the state Department of
Natural Resources says it has found 316 wild deer with the disease in 8
southern counties - Columbia, Dane, Iowa, Kenosha, Richland, Rock, Sauk,
and Walworth. The new IDEXX screening test so far in 2004 has detected
159 deers positive for the disease in 14 additional counties: Chippewa,
Crawford, Dodge, Eau Claire, Grant, Jefferson, LaFayette, Manitowoc, Marinette,
Marquette, Portage, Taylor, Vernon, and Waukesha, state records show. The
Department of Natural Resources (DNR) found chronic wasting disease in
3 bucks shot near Mount Horeb in 2002, marking the first time it was found
east of the Mississippi River. According to the website for IDEXX laboratories
on the HerdChek
test, this is a USDA-approved rapid test for White-tailed deer with
98.8% sensitivity and 100% specificity. Although there may be false positives,
probably no true positives are missed. This kind of an increase raises
some questions. Are there that many false positives? Is the rapid test
detecting the presence of the prion at much lower levels than immunohistochemistry?
Has this disease always been present in cervid populations at undetectable
levels? or has the disease been present, and we have previously written
the deaths off as winter kill, starvation, overpopulation, or some other
term that was appropriate at the time? Killing deer may be the only way
to curb the disease, but even culling may fail to halt the epidemic. In
the 1980s, a herd of captive Colorado mule deer contracted CWD and were
slaughtered : their pens were decontaminated and restocked - but nearly
10 years later, the disease returned. 3 hunters died from CJD in North
America : 2 (one aged 64) from Washington state and the other aged 54 from
Alaska. Washington and Alaska are not necessarily disease-free, but there
is no evidence that the men ate CWD-infected meat. The 1st case of CWD
in Korea (apparently, the 1st CWD case outside north America) involved
a 7-year-old male elk (Cervus elaphus nelsoni) that was clinically
suspected (a 3-week history of body weight loss, emaciation, excessive
salivation, teeth grinding, fever, anorexia, and respiratory distress),
euthanised, and necropsiedref.
Since initial CWD recording in Canada in 1996, it has been diagnosed on
game ranches in Saskatchewan (68 cases in wild deer and a substantial number
of elk found on game farms) and Alberta (5 deers). The 1st case involved
a single elk located on a small game farm facility in southern Saskatchewan,
which had been imported as a yearling, in 1989, as part of a small shipment
of elk originating from the USA. Since began testing in 1997, 31 cases
of CWD have been confirmed, 10 of which were detected in 2002 : 19 mule
deer have tested positive for CWD since testing resumed in the fall of
2003 -- almost double the previous year's total -- signalling that the
disease may be spreading. In 2001, CWD was recorded in wild deer in Saskatchewan.
The import of elk to South Korea is related to the local demand for antlers
(velvet). For over 2000 years people in Asia have been using the skin of
deer antlers, known as deer velvet, as an aphrodisiac bu it doesn't workref=> peste des petit ruminants (PPR) / kata (from the West African pidgin language) / stomatitis-pneumoenteritis complex / pseudorinderpest speak to its importance in West Africa and beyond, including the Middle East and Asia. PPR has an important economic impact and can result in high mortality, especially when small ruminants from different geographical areas are mixed together, thereby promoting the spread to animals without adequate immunity. Stress also plays a role. Typical signs of PPR are mucopurulent nasal discharge, necrotic oral lesions, and gastroenteritis. Until recently an OIE List A disease, it occurs in most African countries south of the Sahara and north of the equator, including countries of the Horn of Africa. Since the late 1980's, the (clinical) disease has gradually spread to the Arabian Peninsula and the Middle East, reported by Iran, Iraq, Israel, Jordan, Kuwait, Lebanon, Oman, Saudi Arabia, Turkey, the United Arab Emirates, and Yemen. A survey in Syria has shown the existence of PPR infection. The disease spread eastwards; outbreaks of PPR are now known to be common in India, Nepal, Bangladesh, Pakistan, and Afghanistan. It causes considerable economic losses, mortality -- particularly in goats -- sometimes exceeding 50% in infected flocks. PPR virus type N4, dated 1996, has been sequenced in Turkey. The presence of the same virus type has been demonstrated in Bangladesh in 1993, India in 1994-96, Nepal in 1995, Pakistan in 1994, Iran in 1994, Saudi Arabia in 1994, and Israel in 1993, 1994 & 1995. A map, showing the world distribution of reported PPR outbreaks during 2003ref. Wildlife does not seem to play a significant role in the epidemiology of PPR; the disease does not infect humans. In September 1997, a national research program based on serosurveillance was launched in Turkey to determine the distribution of PPR. The disease became notifiable in Turkey in October 1997.According to Turkey's monthly reports, cases of PPR have been recorded in sheep and goats in each of the 1st 9 months of 2004, totaling 30 outbreaks so far. The total number for 2003 was 13. None of these reported outbreaks occurred in Thrace. Turkey reported to the OIE that, during 2003, about 656 000 susceptible sheep and goats have been vaccinated with a homologous PPR vaccine. Reportedly, "zoning" has been added, in 2003, to the previously applied control measures. It would be helpful to obtain information on the referred zone (probably Thrace, the European part of Turkey) and whether the said zone has been regarded, so far, free of PPR by the authorities. The Thrace area is regarded as an FMD buffer zone between Turkey and Europe. For decades, livestock there has been subjected to periodical testing for FMD, in close cooperation with the European Commission for FMD. Results of recent serological tests in Thrace for FMD, and official Turkish confirmation -- or otherwise -- of the Bulgarian allegations regarding PPR there, are of importance
- Suidae
- Phacochoerus
-
Phacochoerus
africanus (warthog) : Trichinella
spiralis
- Sus
-
Sus
scrofa (pig, swine, wild boar) : Taenia
solium,
Trichinella
spiralis,
Trypanosoma
brucei gambiense,
Balantidium
coli,
Brucella
melitensis biovar Suis
(Traum's disease : brucellosis with abortion in swine), Mycobacterium
bovis,
Burkholderia
pseudomallei,
Erysipelothrix
rhusiopathiae
(erysipela in animals, erysipeloid in humans), Leptospira
interrogans
serovar pomona,
pseudorabies
virus (PrV) / Aujeszky's disease virus (ADV) / suid herpesvirus 1
(clinical signs of Aujeszky's disease are similar to those of rabies and
prompted the names mad itch and pseudo-rabies. The disease is primarily
found in swine, the natural host, although it may also affect cattle, sheep,
dogs, cats and goats. Wildlife, such as opossums, rodents, skunks and raccoons,
may, on occasion, be infected. Human infections are limited. The disease
is most often found in swine, primarily because of the confined method
of raising pigs. The disease is transmitted through fecal-oral contact
or through nose-to-nose contact. Opportunities for such contact may more
easily occur in this type of swine raising. There is no recommended treatment
for this disease. In certain age groups of swine, vaccination may eliminate
the expression of clinical signs. Test and removal is another method of
eliminating the disease from the premises. The OIE indicates that the last
report from Bolivia of Aujeszky's disease in pigs was in 1998 and was detected
through serologyref),
Nipah
virus,
Influenzavirus
A H1,
Influenzavirus
A H3,
Influenzavirus
A H4,
Influenzavirus
A H7,
Influenzavirus
A H9
: Influenza viruses currently circulating in North American swine are subtypes
H1N1, H3N2, and H1N2ref.
The classical H1N1 viruses have been circulating
in the swine population since the Spanish flu pandemic of 1918ref.
The first SIV, A/SW/IA/15/30, was isolated in 1930 and is antigenically
similar to the 1918 human influenza virus (Shope RE. Swine Influenza. III.
Filtration experiments and etiology. J Exp Med. 1931;54:373–80). From 1930
to 1998, classic H1N1 viruses were the predominantly
isolated subtype from US swine. In 1998, a new SIV subtype H3N2
emerged and became established in the North American swine populationref1,
ref2.
Genetic analysis showed that it was a triple reassortant virus containing
genes from swine, human, and avian influenza viruses. The H3N2
SIV acquired the polymerase basic (PB) protein 1, HA, and neuraminidase
(NA) genes from a recent human virus, the PB2 and polymerase acidic (PA)
protein genes from avian viruses, and the nucleocapsid protein (NP), matrix
(M), and nonstructural (NS) genes from the classic H1N1
swine virusref1,
ref2,
ref3,
ref4.
A year later, reassortment between the H3N2 and classic
H1N1 SIV resulted in a new subtype H1N2,
where the HA of the H3N2 subtype was replaced by
the HA from the classic H1N1 virusref.
This H1N2 subtype caused respiratory disease in swine
and continues to circulate in swine populationsref.
Recently, wholly avian influenza viruses, subtypes H4N6ref,
H3N3, and H1N1ref,
from water fowl were isolated from diseased swine in Canada; however, no
evidence shows that these viruses can be successfully maintained in swine
populations. A new SIV subtype H3N1 that may have
arisen from reassortment of an H3N2 turkey isolate,
a human H1N1 isolate, and currently circulating swine
influenza virusesref.
Although influenza viruses show host-range–specific characteristics, interspecies
transmission of influenza viruses has been well documentedref.
Infection of turkeys with swine influenza viruses seems to be common, and
influenza viruses isolated from turkeys indicated that 73% of turkey influenza
viruses contained genes of swine originref.
Influenza viruses antigenically similar to the classic H1N1
swine virus were found to infect and produce diseases in different turkey
herdsref1,
ref2,
ref3.
Recently, an influenza virus containing 8 genes closely related to those
of A/SW/IN/9K035/99 H1N2 caused an outbreak in a
turkey flock from Missouriref.
Thus far, transmission of turkey viruses to swine populations has not been
reported. SIV subtype H3N1 viruses were previously
isolated in Taiwanese swine; these viruses most likely acquired the HA
from a human H3N2 isolate and the NA from an H1N1
SIV circulating in Taiwanref.
- Demodex phylloides : a species causing mange in swine.
- classical swine fever (CSF) virus / hog choleraref (only 1 serotype) is a contagious List A viral disease of pigs endemic in the wild boar population in Italy (expecially Sardinia), Belgium, Luxembourg, France, and Germany and sometimes spills over into domestic pigs. Most African countries declare to be free of Classical swine fever (CSF) for decades if not generationsref. There is patently a widespread risk of this wildlife disease infecting domestic swine in many countries in Africa." Unfortunately, this has come true in South Africa, a country which has not seen CSF since 1918, now detected and duly notified. Enhanced vigilance is required in other countries in the region. The disease may run an acute, subacute, chronic, or inapparent course, depending on a variety of viral and host factors of which the age of the animals, the virulence of the virus, and the time of infection (pre- or post-natal) are of greatest importance. Adult pigs usually display less severe signs of disease than young animals and stand a better chance of survival. In pregnant sows, the virus may cross the placental barrier and reach the fetuses. In utero infection with strains of the virus of moderate or low virulence can result in what is referred to as the "carrier sow" syndrome followed by prenatal or early post-natal death, the birth of diseased piglets, or an apparently healthy but infected litter. An outbreak of CSF has serious consequences for trade in pigs and pig products, causing severe economic losses. Further details on CSF, its diagnosis and the vaccine, are available in chapter 2.1.13. of OIE's Manual of Standards for Diagnostic Tests & Vaccinesref. CSF does not affect humans. According to article 5 of Directive 2001/89/EC, the main measures in case of confirmation of the presence of CSF in pigs on a holding are:
- 1. all pigs on the holding are to be killed without delay under official supervision and in such a way as to avoid the risk of spread of CSF virus during transport or killing;
- 2. the carcasses of pigs which have died or have been killed are to be processed under official supervision;
- 3. meat of pigs slaughtered during the period between the probable introduction of disease to the holding and the taking of official measures shall wherever possible be traced and processed under official supervision;
- 4. all substances and waste likely to be contaminated, such as feeding stuff, must be subjected to a treatment nsuring the destruction of CSF virus; all single-use materials which may be contaminated, in particular those used for slaughter operations, should be destroyed; these rules shall be applied in accordance with the instructions of the official veterinarian;
- 5. after the pigs have been disposed of, the buildings used for housing the pigs, the vehicles used for transporting them or their carcasses and the equipment, bedding, manure and slurry likely to be contaminated shall be cleaned and disinfected.
- 6. in the case of a primary outbreak of disease, the CSF virus isolate shall be subject to the laboratory procedure laid down in the diagnostic manual to identify the genetic type;
- 7. an epidemiological enquiry shall be carried out.
- African swine fever (ASF) virus (ASFV) is an infectious disease of domestic and wild pigs that affects animals of all breeds and ages, and which is caused by a virus that produces a range of syndromes. Acute disease is characterized by high fever, hemorrhages in the reticuloendothelial system, and a high mortality rate, which, when highly virulent strains are involved, may reach 100%. Infectious virus can survive for several months in fresh and salted dried-meat products. This virus is currently classified as the only member of a family called Asfarviridae; it does not infect humans. ASF is endemic in Ghana; during the period January-November 2004, 20 outbreaks in Central Region, Ashanti, Northern Region and Upper East were reported to the OIE. The current outbreak, in the South, seems to represent a further spread of the disease. It is common in countries in the East Africa such as Mozambique, Tanzania and Zambia. Transmission of ASFV from warthogs to domestic pigs is entirely via the bites of infected ticks, unless the circumstances were very unusual. Warthogs over the age of 2 months are most unlikely to be viraemic and do not therefore shed virus. The "piglets" mentioned are of course warthog piglets, which is unclear from the report. Neonatal warthogs spend the 1st 4-6 weeks of their lives in the burrows, which are populated by large numbers of soft ticks (eyeless tampans) of the Ornithodoros moubata complex, some of which are likely to be infected with ASF virus. The ticks feed on the warthog piglets, which develop high viraemia, although they do not show any signs of disease. Once a domestic pig has been bitten by an infected tick, the rest of the herd will rapidly be infected, as pigs are excellent multipliers and shedders of the virus. The separation between domestic pigs and warthogs is therefore mainly to prevent the domestic pigs from being bitten by infected ticks. Although the ticks normally feed rapidly and drop off the warthogs in the burrows, fairly large numbers of ticks, in particular nymphs, have been found on warthogs. In the control zone in South Africa, warthogs may actually be attracted to sites where pigs are kept, if the separation is inadequate, because it gives them access to feed and water, and they may burrow under fences. Feeding offal from hunted warthogs to domestic pigs is obviously also not a good idea, because the skin, with any ticks that may be attached, could form part of the offal. Virus may also be present in spleen and lymph nodesref. While we tend to see African swine fever more in East Africa, it is not unknown in West Africa. Senegal had a "suspected" OIE report in September of 2004 for which we are still awaiting confirmation. Nigeria experienced an outbreak killing > 50,000 pigs in 2001, and Cameroon lost 75% of the nation's pig population in the late 1980s. Also endemic in Sardinia
- circovirus associated diseases of swine are of increasing concern to producers around the world. Much remains unknown concerning the transmission, pathogenesis, epidemiology, and control of risk factors
- porcine circovirus type 1 (PCV1) was identified for the first time in 1971. It was then regarded as a non-disease-causing agent. It appeared to occur primarily in laboratory tissue cultures.
- porcine circovirus type 2 (PCV2) =>
- postweaning multisystemic wasting syndrome (PMWS) / porcine dermatitis and nephropathy syndrome (PDNS) was initially detected in 1991 in western Canada, while the presence of this disease in Europe was first noticed in France (Brittany) in 1996; however, retrospective studies from several countries indicate PMWS was present in the previous decade. The incurable disease is specific to weaner pigs aged 4-14 weeks and features a progressive loss of weight and appetite, visibly enlarged lymph nodes, respiratory distress, diarrhoea, gastric ulcers, and jaundice. It can vary in severity and virulence, but generally there is a low incidence of disease in affected herds, and a high death rate among those pigs which fall sick (4-10%), but farms with post-weaning mortality up to 60% have been reported. The disease can also be seen in older pigs, particularly finishing pigs that weigh 45-70 kg. Morbidity is typically 5-20 percent among cohorts in the nursery or finishing stages. Mortality in swine that show signs of PMWS often is above 50%. In addition to death loss, PMWS in finishing pigs may prevent, or substantially delay, affected pigs from reaching market weight, which can result in economic loss for the producer. Overseas experience shows that the disease might spread between pig herds through the movement of pigs, and possibly in semen. Guidelines from the EU to control PMWS are: limit litter-to-litter contact of piglets, both through fostering and multi-suckling, and indirectly from shared needles, equipment, and mud; reduce animal stress and susceptibility to disease by limiting exposure to micro-organisms; and practise good management, hygiene and biosecurity on the farm. PMWS is not included within the Office International des Epizooties' list of notifiable diseases, since the etiology and epidemiology of the disease have not been clearly established. Transmission of this disease is believed to be through direct contact. However, fomite, contaminated feeds, semen and biting insects are not clearly understood in the picture of transmission, and more research on these is needed. However, the virus has been found in urine, feces, blood and saliva. It has been found in the semen of infected swine, but the role of semen in transmission of the disease is unclear. There is no treatment for the disease. Antibiotics are generally not recommended in viral diseases, but antibiotics may help prevent secondary bacterial infectionsref
- porcine dermatitis and nephropathy syndrome (PDNS)
- reproductive failure
- porcine respiratory disease complex (PRDC)
- granulomatous enteritis
- necrotizing lymphadenitis
- possibly greasy pig disease / exudative epidermitis : seborrhea of piglets caused by infection of Staphylococcus hyicus through a cut or abrasion of the skin
- association of PCV2 with congenital tremor in piglets is still controversial.
-
swine
vesicular disease (SVD) virus belongs to the enterovirus group of picornaviruses
and is closely related to the human
enterovirus Coxsackie B-5
and unrelated to known porcine enteroviruses. It causes a milder disease
than FMD and causes no mortality. Laboratory tests will readily distinguish
this virus from FMD, vesicular exanthema of swine (a disease of
swine that was seen in 1959; it was caused by a calicivirus and was marked
by vesicles on the snout, lips, tongue, feet, and teats), and vesicular
stomatitis. Pigs are the only natural hosts, although mice have been
experimentally infected, and people have seroconverted when accidentally
infected in the laboratory, so caution is warranted when handling the virus.
Charles Mebus, whose opinion is highly valued -- especially when it comes
to the vesicular diseases -- suggests in the FAD
"Gray Book" that some researchers believe this is a case where a human
pathogen was transferred to pigs. SVD was first diagnosed in Italy and
has occurred in Europe several times during the 1990s including Spain (1993),
Belgium (1993), The Netherlands (1994), and Portugal (1995). The only European
country which has reported SVD during 2005 is Italy (6 outbreaks, last
confirmation 4 Mar 2005ref).
According to Romania's last annual report to the OIE, the SVD has been
absent since 1985.
- porcine reproductive and respiratory syndrome virus (PRRSV) / mystery swine disease emerged in North America and Europe, roughly simultaneously, in the late 1980s. It is also commonly found in Asia. Its spread to Africa really does complete the picture of a pandemic that has relentlessly but not very rapidly spread across a wide swath of the world. The most important question epidemiologically is how the disease spread to South Africa, as new herds are often infected when swine showing no clinical signs are brought into the herd => porcine epidemic abortion and respiratory syndrome (PEARS) / mystery pig disease : a disease affecting pregnant pigs and characterized by fever, anorexia, and respiratory distress followed by unusually high numbers of late-term abortions, stillbirths and other piglets born with respiratory distress, weakness, and neurological conditions such as splayleg. Production losses from the disease are severe. It is a very damaging disease economically, as the fruit of much the investment on a swine farm is lost through abortion and infertility. Requirements for PRRS vaccines can be seen in chapter 2.6.5.
- porcine proliferative enteropathy : transmitted by oral-faecal infection with the bacteria Lawsonia intracellularis. The bacteria cause severe intestinal lesions, diarrhea and gut bleedings which can negatively affect the growth performance in fattening due to reduced weight gains, extra feed costs in growing pigs and increased body weight variation at slaughter. Ileitis is one of the most prevalent diseases worldwide which affects swine production. According to a diagnostic survey by McOrist in 2003, in up to 90% of farms at least one pig was diagnosed to be infected by Lawsonia intracellularis, whereas in a most recent study, the prevalence is even higher (up to 100%). However, the majority of farms are infected sub-clinically i.e. without obvious symptoms, such as diarrhea or sudden deaths, as seen in the clinical form of the disease. Even these sub-clinical infections already affect farm economics negatively. With Ileitis-affected pigs which are poorly gaining weight, the farmer faces considerable economic losses. The economic impact of clinical and sub-clinical forms of Ileitis is estimated to cost between €1.3 and €18.5 per affected pig depending on the severity and duration of the disease. Enterisol® Ileitis (source : Boehringer Ingelheim Animal Health) is approved for the active immunization of pigs against Lawsonia intracellularis throughout the European Union. All grow/finish pigs, breeding sows and gilts are licensed to be vaccinated with Enterisol® Ileitis. In 2001, Enterisol® Ileitis has been launched in North America and is furthermore licensed in Mexico, Brazil and the Philippines. Since 2001, approximately 100 million pigs have been vaccinated worldwide, establishing Ileitis control as an essential part of professional pig health management.
- porcine stress syndrome / herztod : sudden death of a pig in response to a stressor such as fighting, transport, or malignant hyperthermia, or as part of a drug reaction. Susceptibility in most cases is inherited as an autosomal recessive gene
- vitamin E–selenium deficiency syndrome : a deficiency disease of pigs whose diet is low in vitamin E and selenium, most commonly rapidly growing, recently weaned piglets. It usually manifests as either hepatosis dietetica or mulberry heart disease, and affected animals may die suddenly during exercise.
- mulberry heart disease : a form of vitamin E–selenium deficiency syndrome in pigs, characterized by subepicardial hemorrhaging, myocardial necrosis, and often death
- diamond skin disease : the urticarial form of swine erysipelas.
- dancing or shaker pig : a pig suffering from congenital tremor syndrome.
- porcine enterovirus / ecsovirus : a species of viruses of the genus Enterovirus, separable into eleven serotypes, that are normal inhabitants of the intestinal tract of swine but may cause infectious porcine encephalomyelitis
- vomiting and wasting disease / Ontario encephalitis / hemagglutinating encephalomyelitis virus disease of pigs : a disease of pigs caused by infection with the hemagglutinating encephalomyelitis virus; the virus is endemic in many parts of the world and only occasionally causes symptoms. The disease varies from acute encephalomyelitis that can be fatal in a few days to anorexia, vomiting, and wasting that can last for 2-3 weeks without being fatal
- Glasser's disease / infectious porcine polyarthritis or polyserositis : a disease of young pigs, caused by infection by Haemophilus parasuis; symptoms include swelling of the hocks or knee joints or both, accompanied by fever and lameness; severe cases may progress to neurological problems with disinclination to move, convulsions, and death
- edema disease / bowel or gut edema / Escherichia coli enterotoxemia : enterotoxemia in recently weaned piglets caused by a strain of Escherichia coli that normally colonizes the small intestine; characteristics include edema in various parts of the body, with neurological signs such as circling and ataxia
- inclusion body rhinitis : mucopurulent rhinitis and sinusitis of young pigs due to infection with a cytomegalovirus; severe cases may be marked by atrophy of the turbinate bones and distortion of the snout, sneezing, stunting of growth, and, histologically, by the presence of inclusion bodies in scrapings of the nasal mucous membranes.
- atrophic rhinitis of swine : a disease of young swine caused by severe persistent inflammation of the nasal mucosa; severe cases may result in marked atrophy of the turbinate bones and lateral displacement of the snout. The primary inflammatory reaction may be caused by a variety of agents, including a virus
- porcine myocarditis (PMC)ref only affects unborn piglets and growing swine up to 5 weeks of age and has not been detected in any adult pigs intended for human consumption. It has been limited to 2 piggeries in NSW, both of which are owned and operated by the same company. Clinically PMC presents as an increase in stillbirths and pre-weaning mortalities. There is also a variable but significant increase in the incidence of mummified foetuses. The gross pathological changes consist of small pale areas in the myocardium. There is often evidence of cardiac enlargement and an increase in the volume of body fluids, consistent with congestive heart failure. Histologically there is a non-suppurative myocarditis. It is believed that the syndrome is due to a viral infection predominantly, if not exclusively, occurring in utero. PMC is not a recognized exotic (FMD, PRRS, Aujesky's disease, classical swine fever, and Menangle virus) or endemic (EMC, porcine parvovirus, PCV1, PCV2, and BVDV) disease. Electron microscopy on affected myocardium and lungs has detected small virus-like particles ranging from 19-27 nm, fastidious in its growth requirements. PMC is already resolving itself, with piglet losses due to the disease approaching zero. No impact on human health or food safety has been identified. Pigs grown to market weight have shown no sign of the disease at slaughter
- transmissible gastroenteritis (TGE) is an enteric disease of pigs caused by TGE virus (TGEV), a member of the Coronaviridae. TGEV multiplies in, and damages the enterocyte lining of, the small intestine, producing villous atrophy and enteritis. Watery, foul-smelling diarrhea and vomiting occur in pigs of all ages. Morbidity and mortality in growers and finishing pigs is tolerable but can be explosive and fatal in piglets less than 3 weeks of age. Extra-intestinal sites of virus multiplication include the respiratory tract and mammary tissues, but the virus is most readily isolated from the intestinal tract and from feces. As TGE is a contagious disease that can occur as explosive epizootics, rapid diagnostic methods for its confirmation are particularly important. The disease can also take the form of a low-level endemic problem of post-weaning diarrhea, which is more difficult to diagnose. Virus may be identified by virus isolation in tissue culture, electron microscopy, various immunodiagnostic assays, and, more recently, by specific detection of viral RNA. The most commonly employed rapid assays are probably the immunodiagnostic ones,
- porcine epidemic diarrhea, another enteric disease caused by a serologically distinct coronavirus (porcine epidemic diarrhea virus) that, nevertheless, has an identical appearance under the electron microscope. Diagnostically, immune electron microscopy circumvents this problem
- mastitis-metritis-agalactia / lactation failure in swine / farrowing fever : a variable syndrome in sows with agalactia occurring during the first two days after they have given birth; it may be accompanied by mastitis with fever, anorexia, and increased respiratory and heart rates, and occasionally by metritis with a vaginal discharge
- postweaning diarrhea / weanling pig scours : potentially fatal diarrhea in piglets just after they are weaned; causes may be allergies to ingredients of the new diet or intestinal infection, such as by a strain of Escherichia coli
- porcine or swine babesiosis :
- Babesia perroncitoi : a species causing swine babesiosis in Africa; the vector is unknown.
-
Babesia trautmanni : a species causing swine babesiosis in Europe,
Asia, Africa, and Central and South America; transmitted by the tick Rhipicephalus
sanguineus.
- Tayassuidae; Pecari
- Pecari tajacu (a.k.a. collared peccary, Tayassu tajacu, Tayassu angulatus, javelina) resembles a wild pig, in that it has cloven feet, a pig-like snout and coarse, thinly distributed hair. But its physiology differs from that of pigs. Their main food is prickly pear cactus, or other succulent cacti, and they are desert dwellers. They are fascinating to observe, as they are both affectionate to their family members and fiercely protective of them.
, Japanese encephalitis virus (JEV)
(a trial vaccination programme for pigs against JEV is being considered
in Hong Kong), Hepatitis E
virus (HEV)
(1.9% of livers), encephalomyocarditis
virus (ECMV)
(encephalomyocarditis virus (ECMV) disease
: a viral disease that usually occurs in rodents but is transmissible to
other animals, especially pigs. It is often clinically inapparent but sometimes
causes reproductive failure in young female pigs or encephalomyocarditis
in various species, which can be fatal), Bacillus
anthracis
(pigs, though moderately resistant to anthrax, do get infected either through
contaminated pig feed or by feeding on the carcasses or organs of dead
animals -- vide "Peyton Place" for those who can remember the book -- .When
outbreaks are still occurring outside the usual "Anthrax season" it is
very wise of the local authorities to forbid boar hunting. Recently Russia
has been witnessing increasing numbers of anthrax outbreaks in pigs. Their
commonest lesions are in their throats, especially with abrasive feed;
the more abrasive the feed mix, the higher the incidence) Pigs are rarely
vaccinated unless they are at risk from contaminated feed or from an ongoing
outbreak, as they are relatively resistant. In poor rural areas, pigs become
infected from access to dead animals or their viscera. Some 30 years ago
in the UK, there was a prolonged outbreak among sheep and pigs on a farm
because, as the sheep died, the pigs got to the carcasses before the farmer
could remove them. Pigs dying of anthrax is a marker event for a more widespread
problem. How this pig was found to be sick and submitted for analysis is
not reported. These Russian animal cases are unfortunately too often discovered
as the result of human cases. One can optimistically hope that this event
was in the proper order, livestock without human cases)
Other diseases not transmissible to humans :
of OIE's manual for diagnostic tests and vaccines for terrestrial animalsref. Prevention: Ingelvac® PRRS MLV (source : Boehringer Ingelheim Animal Health)
particularly, enzyme-linked immunosorbent assays (ELISAs) on feces, and fluorescent antibody tests on cryostat sections of intestine. Detection of virus by reversed passive hemagglutination has also been describedref. TGE is well-known in most swine-producing areas of the world. During 2003, the presence of TGE was reported by 9 OIE member countries: Belarus, Croatia, France, Germany, Mexico, Romania, Russia, Slovenia, and Taiwan. Lebanon is the only Middle-Eastern country where the disease has been reported in recent years, namely during 1995-1998 : reportedly, the disease has not been detected there since 1998. During 2004 in Israel
Web resources : Pig Health by Mike Meredith
-
Camelidae
(camels) : camelpox virus,Taenia
solium,
Yersinia
pestis
- Camelus
-
Camelus
dromedarius (dromedaries) : Trichostrongylus
probolorus,
Trichostrongylus
vitrinus
- Lama
